J Reconstr Microsurg 2002; 18(7): 579-584
DOI: 10.1055/s-2002-35095
Copyright © 2002 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

Effects of Late Loss of Arterial Inflow on Free Flap Survival

Christopher J. Salgado1 , Andrew Smith2 , Sunmi Kim2 , Jim Higgins2 , Amir Behnam2 , H. Raul Herrera2 , Joseph M. Serletti2
  • 1Plastic Surgery Section, Darnall U.S. Army Hospital, Ft. Hood, TX
  • 2Division of Plastic Surgery, University of Rochester, Rochester, NY
Further Information

Publication History

Publication Date:
29 October 2002 (online)


Greater than 80 percent of free flap thromboses have been shown to occur within the first three postoperative days, warranting immediate re-exploration and restoration of adequate vessel patency. The infrequency of thromboses beyond this period is reflected in the lack of reported cases in the literature and the absence of accepted guidelines for the treatment of such delayed complications. A single study reported free flap survival in vessel thromboses only when encountered after postoperative day (POD) 7 in a pig model. Since 1990, over 800 free tissue transfers have been done at the University of Rochester. A total of ten cases of late (defined as after POD 7) arterial inflow loss were identified and examined. A retrospective chart review recorded patient demographics, site of tissue defect, free tissue transferred, major co-morbidities, preoperative XRT, timing of arterial inflow loss, nature of inflow loss, and flap survival. The mean POD of arterial inflow loss was 53 days (range: 8 to 166). The mean age of patients was 58 years. No major co-morbidities correlated with late arterial inflow loss. Loss of inflow occurred as anastomotic rupture (5), occlusion of recipient bypass graft in lower extremity cases (3), primary donor arterial thrombosis (1), and pedicle avulsion during re-exploration for seroma (1). Five flaps survived, one sustained partial necrosis, and four were completely lost. Of the five surviving flaps, three were inset into healthy recipient sites. One was utilized on a dysvascular lower extremity, and another was used in an irradiated neck defect. Of the four failed flaps, all were placed in recipient beds compromised by radiation, ischemia, or scarring. Two exemplary case reports are presented. The timing of late loss of arterial inflow does not appear to be the primary determinant of free tissue survival. The condition and quality of the recipient site plays a large role in survival of these flaps. Ischemic, irradiated, and scarred beds are inadequate in providing late flap neovascularization, compared to healthy recipient sites. When encountering late loss of arterial inflow in flaps placed on such compromised beds, the microsurgeon should not anticipate survival based on surrounding vessel ingrowth. More aggressive salvage attempts may be warranted.