Nature and management of duplex abnormalities encountered during infrainguinal vein bypass grafting

This study was undertaken to evaluate the application of duplex scanning during infrainguinal vein grafting procedures to verify vein conduit preparation, anastomotic patency, and graft hemodynamics.

Between 1991 and 1995, 275 infrainguinal vein bypasses (in situ, 114; reversed, 82; nonreversed translocated, 48; spliced alternative/arm vein, 31) to the popliteal (n = 116) or an infrageniculate artery (n = 159) were scanned during surgery for sites of color Doppler flow abnormality. Duplex-detected defects were graded with peak systolic velocity and velocity ratio criteria. Sites that demonstrated highly disturbed flow (peak systolic velocity > 180 cm/sec, velocity ratio > 2.4) were immediately revised by direct repair, patch angioplasty, or interposition grafting.

Intraoperative duplex scanning prompted revision of 50 abnormalities in 43 of the 275 grafts (16%), including 32 vein and seven anastomotic stenoses, nine vein segments with platelet thrombus, and two bypasses with low flow. The intraoperative revision rate was lowest (p < 0.02) for reversed saphenous vein bypasses (7%) compared with other grafting techniques (in situ, 20%; nonreversed translocated, 15%; spliced alternative vein, 23%). The revision rates of popliteal and tibial bypasses were similar (14% vs 17%). A normal result shown by intraoperative scan (235 bypasses) was associated with a low 90-day thrombosis (0.4%) and revision (2%) rate, whereas six of 15 grafts (40%) with residual and 13 of 25 grafts (52%) with unrepaired duplex abnormalities required corrective procedures (p < 0.001). One graft failed within 3 months (secondary patency rate, 99%).

Intraoperative duplex scanning accurately predicted the technical adequacy of infrainguinal vein grafts and was particularly useful in assessing bypasses constructed with valve lysis techniques or alternative veins. Early graft revisions indicated by duplex monitoring for thrombosis or stenosis were the result of a progression of residual defects and platelet thrombus formation rather than inadequate graft run-off flow.