INTRODUCTION: Free-flap ischemia is a dreaded complication. There has been little written about specific factors leading to ischemic events in free-flaps and even less regarding successful management options. The purpose of this study was to examine the etiology of free-flap ischemia in a large series of autologous breast reconstructions and to highlight treatment options. METHODS: A retrospective chart review of all patients who underwent free-flap breast reconstruction over a ten-year period was performed. Patients experiencing intra or postoperative free-flap ischemia leading to reoperation were identified. RESULTS: There were 23 reconstructions with at least one ischemic episode each in 23 patients. Obesity was present in 6 patients, controlled hypertension in 3 patients, and controlled diabetes in 2 patients. Five patients had a history of cigarette smoking. Free TRAM reconstructions were performed in 14 patients, superior gluteal free-flaps in 8 patients, and there was one tensor fascia lata reconstruction. There were a total of 28 ischemic events. The first ischemic event for each flap occurred: intraoperatively (7), day of surgery (4), POD#1 (8), and POD#5, 7, 9, and 13 (1 each). One ischemic event per flap occurred in 19 cases. In 3 cases there were two ischemic events per flap, and in one case there were 3 ischemic events. Ischemic events were categorized as venous thromboses (14), arterial thromboses (8), simultaneous arterial and venous thromboses (2), arterial vasospasm (2), and mechanical obstruction/no thrombosis (2). Etiology of ischemic events were: size discrepency (10), technical/occult vessel injury (9), mechanical (obesity, seroma, muscle compression) (3), trauma (2), pedicle tension (1), pedicle redundancy (1), hypovolemia/pressors (1), and vein graft phlebitis (1). Operative interventions were: resection of anastamosis/portion of vessel with damaged intima (10), change of recipient vessel (8), thrombolysis (3), anastamosis/vessel resection with vein graft placement (2), anastmotic exploration (2), flap reposition (1), resection of pedicle redundancy (1), evacuation of seroma (1), removal of muscle compression (1), and volume replacement (1). There were 3 total and one partial flap losses. Other complications included hematoma (6), mild or moderate fat necrosis (3), cellulitis (3), and seroma (1). There were no patient deaths. CONCLUSIONS: In this series, one of the major factors responsible for microvascular thrombosis was vessel size mismatch (particularly when a large flap vein was anastamosed to a smaller draining vein). Based on our findings, we feel that a discrepancy of greater than 2:1 should be avoided by using larger alternative recipient vessels. A second major etiologic factor was related to presumed minor technical errors and occult vessel damage in either in the flap vessels or in the recipient vessels. In the absence of other problems, resection of the involved area with possible thrombolysis or vein grafts should be used. If possible, thrombolytics should be delivered to the flap by intraluminal injection into the arterial system proximal to any thromboses and excess thrombolytics can be removed by draining the venous circulation. Mechanical and volume issues, along with vasospasm, were responsible for a third group of ischemic events. Therefore, postoperative monitoring and medical optimization are critical to success.