Therapeutic options for acute thromboscd in situ saphenous vein arterial bypass grafts Dennis F. Bandyk, MD, Jonathan B. Towne, MD, David D. Schmitt, ME}, Gary R. Seabrook, MD, and Thomas M. Bergamini, MD, Milwaukee, Wis. Abnormalities of the conduit, otfflow tract, and graft hemodynamics are important elements in the mechanism of vein graft thrombosis, and their role must be defined when planning reoperation. In a consecutive series of 353 in situ saphenous vein bypass graftings performed for occlusive or aneurysmal disease, graft thrombosis occurred in 18 (5%) patients during the perioperative period and unexpectedly in 14 (4%) patients after discharge from the hospital. Assessment of graft hemodynamics (calculation of blood flow velocity) before thrombosis was helpfid in predicting success after graft revision. Five grafts with known low flow (systolic flow velocity a We have advocated use o f Doppler-derived blood flow velocity measurements to exclude technical error at operation and detect low-flow states in grafts after operation indicative of a "graft stenosis" or atherosclerotic disease progression.4"6 Despite implementation of a graft surveillance protocol based on noninvasive hemodynamic testing, unexpected
From the Surgical Service, Veterans Administration Medical Center, and the Department of Surgery, The Medical College of Wisconsin. Supported by the Veterans Administration. Presented at the Thirteenth Annual Meeting of the Midwestern Vascular Surgical Society, Chicago, Ill., Sept. 29-30, 1989. Reprint requests: Dennis F. Bandyk, MD, Department of Surgery, MCMC, 8700 W. Wisconsin Ave., Milwaukee, WI 53226. 24/6/19226 680
graft thrombosis has occurred. This observation indicates that some mechanisms of graft thrombosis can escape detection despite hemodynamic moni, toting. Identification of the mechanism of vein graft failure is critical since thrombectomy alone or with veinpatch angioplasty will not salvage most thrombosed bypass grafts. 7'8 Segregation of in situ bypass grafts into low- or normal-flow states based on blood flow" velocity measurements may be helpful in defining mechanisms of graft failure and thus facilitate decision making regarding suitability of patients for secondary procedures. Graft thrombectomy alone or prosthetic replacement are not likely to be successful if inadequate outflow is the mechanism of throm, bosis. In this report we detail our experience of reoperation for acute thrombosis of in siva saphenous vein bypass grafts after 353 consecutive procedures performed over 9 years. The incidence, mechanisms o f thrombosis (proven and hypothesized), and outcome of this complication were correlated with hemodynamic data recorded from the in siva vein bypass graft before the thrombotic event.
Volume 11 Number 5 May 1990
MATERIAL AND METHODS From January 1981 to July 1989, 353 in situ saphenous vein bypass grafts for occlusive or aneurysmal disease were placed in 328 patients. The study included 264 men and 64 women whose ages ranged from 42 to 92 years (mean, 63 years). Indications for bypass grafting included critical limb ischemia (n = 321, 91%), life-style limiting clandication (n = 18, 5%), and popliteal artery aneurysm (n = 14, 4%). In all but 15 limbs the proximal anastomosis was to the common femoral artery. Other sites of vein bypass graft origin included aortofemoral or femoral-femoral prosthetic grafts (n = 5), and ' popliteal (n = 6) or superficial femoral arteries (n = 4). The site of the distal anastomosis was selected based on angiographic criteria of the leastdiseased artery with patency to the ankle or pedal arch. Eleven patients required interposition of reversed saphenous or cephalic vein to replace sclerotic vein segments or obtain sufficient graft length for anastomosis to the outflow artery. Distal anastomosis was to an infrapopliteal artery in 227 limbs, the below-knee popliteal artery in 120 limbs, and an above-knee or isolated popliteal artery segment in 6 limbs. The technique of in situ bypass grafting has not been modified from our previous reports, t'9 The procedure was performed by means of an open technique with exposure of the entire length of saphenous vein. Intraoperative pulsed-Doppler spectral analysis with a high (20 MHz) frequency Doppler flowmeter, routinely used since 1983, and more recently duplex color flow imaging were used to assess technical adequacy of the bypass graft and to define the hemodynamics of graft blood flow. Measurement of blood flow velocity in the in situ venous conduit was performed under basal flow conditions approximately 20 minutes after restoration of graft blood flow. The technique of intraoperative pulsed-Doppler spectral analysis including selection of recording sites in thc ,venous conduit has been previously described. 1,4,1° Intraoperative studies served as a baseline for comparison with postoperative studies obtained from the identical graft segments by use of duplex scanning. Operative arteriography was used to confirm a technically satisfactory distal anastomosis and patent outflow tract. All patients underwent serial noninvasive hemodynamic testing after operation (intervals of 1 and 7 days, 6 weeks, and every 3 months thereafter). Testing methods included measurement of resting limb arterial pressure by the transcutaneous Doppler ultrasonographic flow detection technique and calcu-
In situ saphenous vein graft thrombosis 681
lation of blood flow velocity from above- and belowknee graft segments by means of (1) a transcutaneous, continuous wave Doppler spectral analysis (5 MHz probe frequency, 45 degree Doppler angle to the skin) if the graft was immediately beneath the skin, or (2) duplex scanning when the graft was more deeply positioned in subcutaneous tissue and more accurate Doppler angle assignment was desired. Graft patency was determined by physical examination, decrease in resting ankle systolic blood pressure as calculated by the ankle-brachial systolic pressure index (ABI), and duplex scanning. An interval decrease in ABI greater than 0.2 was used as a criterion for arteriography or duplex scanning to assess graft patency. Since the focus of this report was the management of acutely thrombosed in situ saphenous vein grafts and indirectly the effectiveness of hemodynamic graft surveillance, six patients who came for treatment weeks after graft failure and had not participated in the surveillance protocol or were lost to follow-up were excluded from the study. Also excluded from the analysis were four patients identiffed by hemodynarnic surveillance to have low graft flow (systolic blood flow velocity less than 45 cm/sec) caused by occlusive lesions in the outflow tract not amenable to revision (verified by arteriography). Graft thrombosis in this cohort was expected and occurred at varied time intervals ranging from 3 to 14 months after documentation of the low-flow state. These patients were not considered for reoperation after graft failure, and all required above- or below-knee amputation. We have previously reported our experience with revision of hemodynamically failing but patent in situ bypass grafts identified by duplex scanning and/or arteriography to have a correctable graft stenosis, and this concept is not addressed in this report? RESULTS Perioperative graft thrombosis. Eighteen (5%) of the 353 in situ saphenous vein grafts thrombosed within 30 days of operation. All but one had as outflow an infrapopliteal (posterior tibial, 9; anterior tibial, 4; peroneal, 3) artery or isolated popliteal artery segment. Critical ischemia was the indication for bypass grafting in all patients. Fourteen grafts occluded within 24 hours of the primary operation. The frequency of early graft failure has remained constant over the duration of this series (Fig. 1). The incidence of perioperative graft thrombosis of 8% observed after the first 87 in situ bypasses (years 1981 to 83) was not significant different (p = 0.2, chi square) from the 4% incidence observed after the
Journal of VASCULAR SURGERY
682 Bandyk et al.
No. of grafts 125
III No. ot in situ bypasses N 30-day thrombosis
100 75 50 25 0
81-83
84-85
86-87
88-89
YEAR Fig. 1. Incidence of perioperative (30-day) thrombosis in a consecutive series of 353 in sire saphenous vein arterial bypass grafts performed during a 9-year period (1981 to 89).
Table I. Mechanism of thrombosis, intraoperative graft blood flow velocity, treatment, and outcome of in situ saphenous vein graft failure within 30 days of operation Mechanism of thrombosis
No.
Inadequate outflow
8
Abnormal venous conduit
5
Technical error Anastomoticocclusion
2
Vein-graft torsion Hypercoagulablestate Total
1 ~ 18
Vp* (cm/sec)
38, 18, ND, ND 30 40 26, 30 35 65, 80, 85 33 33 40 72 60, ND
Secondaryprocedure
No. patent
Thrombectomy-4 Graft translocation Sequential bypass No revision-2 Thrombectomy Graft replacement-3 Graft translocation
0 i 1 0 0 3 1
Graft translocation Vein-patch angioplasty Local revision Thrombectomy
1 1 1 _0 9
ND, not determined.
*Vp, maximumsystolicblood flow velocitymeasuredin distal graft segmentat operation.
last 103 procedures (years 1988 to 89). Correlation of the mechanisms of thrombosis with intraoperative graft hemodynamics and outcome of graft revision are summarized in Table I. Overall, patency was restored and limb ischemia was relieved by conduit revision or replacement in 9 of the 18 patients. Assessment of vein bypass hemodynamics was performed at operation in 15 of 18 patients with early graft thrombosis. In 10 bypass grafts, a low blood flow velocity (systolic velocity o f 40 cm/sec or less) was measured in the distal vein graft segment.
Mechanisms of failure o f these low-flow grafts included inadequate outflow (n = 6), technical error (n = 2), and abnormal venous conduit (n = 2). Thrombectomy alone did not restore patency unless the outflow tract was also modified. O f note, only two other grafts with low flow did not thrombose, the low blood flow velocity in these bypass grafts was attributed to large (5 mm or greater) vein di.~ ametcr. Replacement ofthrombosed small (3 mm or less) diameter, or previously vein-patched graft segments
Volume 11 Number 5 May 1990
In situ saphenous vein graft thrombosis 683
Fig. 2. A, Intraoperative arteriogram of an situ saphenous vein bypass to the distal posterior tibial artery (closed arrow). Sclerotic vein segment below the knee revised with vein-patch angioplasty (curved arrow) after pulsed-Doppler spectral analysis identified abnormal flow pattern as a result of platelet aggregation. After revision, low blood flow velocity (Vp = 33 cm/sec) measured in distal graft segment. B, Intraoperative arteriogram of in situ graft after revision by thrombectomy and translocation of the venous conduit to an isolated popliteal artery segment. Reoperation performed within 12 hours of the primary procedure. Blood flow velocity in distal vein graft was 60 cm/sec. Bypass graft remains patent at 3 years, was successful when the prior level of graft blood flow velocity was adequate (greater than 40 cm/sec, antegrade flow throughout pulse cycle). Mechanisms of thrombosis in five grafts with normal intraoperative hemodynamics included abnormal venous conduits (n = 2), graft torsion, and heparin-induced ,platelet aggregation. Reoperation did not restore vein graft patency in both patients with unrecognized coagulopathy. Of note, translocation of the distal anastomosis to a proximal arterial segment (popliteal artery, 2; posterior tibial artery, 1) successfully relieved critical limb ischemia in three patients whose grafts failed because of poor quality vein or anastomotic occlusion (Fig. 2). Graft replacement with a polytetrafluoroethylene (PTFE) prosthesis was necessary in only one patient when repeated thrombec-
tomy failed to restore patency of the venous conduit. Two patients judged to have inadequate outflow to sustain graft patency did not undergo reoperation. Operative (30-day) mortality was 2.5% (eight patients). One patient developed infection involving the venous conduit and necessitated excision of the bypass graft. For the entire series, 342 (97%) of the 353 in situ bypass grafts were patent when the patient died during the postoperative preiod or was discharged from the hospital. Seven of nine patients with early in situ graft failure required above- or below-knee amputaton. Of the nine bypass grafts salvaged by a secondary procedure, three vein grafts, all to an infrapopliteal artery, occluded within i year. Progression of atherosclerosis in the outflow artery was felt to be the mechanism of failure.
yournaiof VASCULAR SURGERY
684 Bandyk et al.
Table II. Graft hemodynamics before thrombosis, mechanism of thrombosis, treatment, and outcome of unexpected in situ saphenous vein graft failure occurring more than 30 days after primary operation Mechanism of thrombosis Low-flow state (Vp less than 45 cm/sec) Known "graft stenosis"
No.
5
Diseased outflow tract Normal graft hemodynamics (Vp greater than 45 cm/sec) -documented within 3 prior months Thromboembolism
2
FaiRed "jump graft" Unknown -documented greater than 3 months prior Probable "graft stenosis" Total
1 1
4
1 14
Secondaryprocedure
No. patent
Thrombolysis/graft revision-2 Thrombolysis/ PTA~- 1 PTFE+, replacement-2 PTFE replacement-2
2 1 2 0
Thrombolysis/Thrombectomy-2 Thrombectomy/ aneurysm repair-2 PTFE replacement PTFE replacement
2 2 1 1
PTFE replacement 12
~PTA, Percutaneous transluminal angioplasty. tPTFE, Polytetrafluoroethylene.
Late graft thrombosis despite hemodynamic surveillance. After discharge from the hospital, 14 (4%) of 340 in situ bypass grafts thrombosed unexpectedly during a follow-up period that ranged from 3 to 92 months. All occlusions occurred within 1 year of the primary operation or a secondary procedure for graft stenosis. Twelve of the failed grafts were anastomosed to an infrapopliteal artery, and two had a below-knee popliteal artery as outflow. Graft hemodynamics before thrombosis, mechanism of thrombosis, treatment, and outcome of these unexpected graft failures are summarized in Table II. Reoperation was successful in relieving limb ischemia in 12 of the 14 patients, although patency of the in sire venous conduit was restored by thrombolysis (intraarterial urokinase infusion) or direct surgical thrombectomy in only six patients. The most common (n = 6) secondary procedure was graft replacement by means of a PTFE prosthesis. In general, if the secondary procedure corrected the mechanism of thrombosis, prolonged graft patency was observed. Prosthetic replacement of two failed in situ grafts with known low flow as a result of diseased outflow tracts did not remain patent, and both patients required below-knee amputation. In contrast, prosthetic replacement of in sire bypass grafts that occluded as a consequence of thromboembolism, known or presumed graft stenosis, or an unknown cause was successful if normal graft hemodynamics, indicative of adequate graft runoff, had been previously documented by noninvasive testing. Two patients who had undergone prior revision
of a "graft stenosis" with normalization of graft hemodynamics (increase in systolic flow velocity to greater than 45 cm/sec, ABI greater than 0.9) developed unexpected graft failure within 9 months, presumably because of a recurrent stenosis of a patch angioplasty and occlusion of a "jump graft" (Fig. 3). Prosthetic graft replacement was successful in relieving ischemia in both patients. Hemodynamic studies of the 5 or 6 m m diameter PTFE replacement grafts demonstrated a blood flow velocity in the range of 40 to 65 cm/sec. During follow-up, three PTFE replacement grafts failed at postoperative time intervals of 6 weeks, 9 and 14 months. The PTFE graft that failed at 6 weeks had a flow velocity of 40 cm/sec and thrombosed 2 weeks after discontinuation of oral anticoagulation (sodiuna warfarin) because of gastrointestinal bleeding from esophagitis. Two of six veingrafts that underwent thrombolysis/thrombectomy alone or in combination with autologous vein revision thrombosed at 6 and 24 months. Overall, 7 of 14 patients operated on for unexpected graft ~rombosis have maintained patency of the arterial bypass graft with follow-up ranging from 9 to 36 months.. (mean 14 months). DISCUSSION These results confirm in situ saphenous vein bypass grafts that occlude after operation can be treated effectively by reoperation. Limb ischemia was re-lieved in 21 (66%) of a2 patients by a variety of secondary procedures including thrombolysis or thrombectomy, revision with autologous vein, or
Volume 11 Number 5 May 1990
In situ saphenous vein graft thrombosis 685
Fig. 3. (Left) Normal intraoperative arteriogram of femoral-anterior tibial in sire saphenous vein bypass graft. Blood flow velocity in the distal vein graft of 55 cm/sec in normal range. (Middle) Arteriogram obtained 10 days after surgery demonstrated antegrade occlusion of the distal anastomosis (arrow). Low (35 cm/sec) blood flow velocity in distal graft prompted "jump graft" revision to dorsalis pedis artery: (Right) Normal intraoperative arteriogram of femoropopliteal PTFE bypass graft (curved arrow) performed for unexpected in sire thrombosis occurring 2 weeks after discharge from the hospital. Systolic blood flow velocity of 45 cm/sec in PTFE conduit. Graft remains patent at 12 months. prosthetic replacement. If the reoperation corrected .the underlying mechanism of graft thrombosis, was appropriately performed, and restored a bypass graft with normal hemodynamics, long-term patency resulted. Decision making regarding the mechanism of graft thrombosis and thus which restorative procedure, if any, was best suited for each patient was facilitated by prior evaluation of graft hemodynamics. Thrombectomy alone did not restore graft patency when the mechanism of thrombosis was (1) an abnormal venous conduit with traumatized, thrombogenic luminal surfaces or (2) low flow as a result of diseased outflow arteries. In these circumstances the abnormal venous segment should be replaced, preferably with autologous vein, and arterial anatomy of the limb should be reviewed for alternative or additional outflow sites of the bypass graft. An operative strategy that involves modification of the graft runoff when a low-flow state in the graft is documented rather than relying on thrombectomy alone should improve the outcome of graft revision after unexpected thrombosis. Perioperative graft thrombosis is always an usa-
expected complication and as such provokes consternation and dismay in both the patient and surgeon. In a recent report of 1000 consecutive in situ saphenous vein bypass graftings, Leather et al. ~1 reported the incidence of pcrioperative thrombosis was 4.4% for grafts to the below-knee popliteal artery, 3.4% for grafts to the proximal tibial arteries, and 7.8% when grafts are anastomosed to a distal tibial artery. Our experience also confirmed thrombosis of an in situ bypass graft within 30 days of operation was uncommon (incidence, 5%), but we found the incidence of perioperative thrombosis was less (p < 0.02, chi square = 6.5) for[grafts anastomosed the below-knee popliteal artery (0.8%, 1 of 120) compared to infrapopliteal vein bypass grafts (7%, 16 of 227). Our results support the use of intraoperative Doppler ultrasound to confirm technical adequacy and sufficient graft blood flow to strstain patency, and provide further evidence that quality of the venous conduit and status of the outflow tract are important elements in the mechanisms of vein graft failure. Using pulsed Doppler spectral analysis and more recently duplex color flow imaging at opera-
686 Bandyk e~ aI.
tion, we have identified residual lesions (intact valve cusps, anastomotic stricture, platelet aggregation in the venous conduit) that warranted correction in approximately 5% of cases) Duplex color flow imaging has the advantage of allowing assessment of blood flow patterns along the entire length of the reconstruction. This capability facilitates intraoperative assessment and should prove to be useful in evaluating the adequacy of a small (
From the Surgical Service, Veterans Administration Medical Center, and the Department of Surgery, The Medical College of Wisconsin. Supported by the Veterans Administration. Presented at the Thirteenth Annual Meeting of the Midwestern Vascular Surgical Society, Chicago, Ill., Sept. 29-30, 1989. Reprint requests: Dennis F. Bandyk, MD, Department of Surgery, MCMC, 8700 W. Wisconsin Ave., Milwaukee, WI 53226. 24/6/19226 680
graft thrombosis has occurred. This observation indicates that some mechanisms of graft thrombosis can escape detection despite hemodynamic moni, toting. Identification of the mechanism of vein graft failure is critical since thrombectomy alone or with veinpatch angioplasty will not salvage most thrombosed bypass grafts. 7'8 Segregation of in situ bypass grafts into low- or normal-flow states based on blood flow" velocity measurements may be helpful in defining mechanisms of graft failure and thus facilitate decision making regarding suitability of patients for secondary procedures. Graft thrombectomy alone or prosthetic replacement are not likely to be successful if inadequate outflow is the mechanism of throm, bosis. In this report we detail our experience of reoperation for acute thrombosis of in siva saphenous vein bypass grafts after 353 consecutive procedures performed over 9 years. The incidence, mechanisms o f thrombosis (proven and hypothesized), and outcome of this complication were correlated with hemodynamic data recorded from the in siva vein bypass graft before the thrombotic event.
Volume 11 Number 5 May 1990
MATERIAL AND METHODS From January 1981 to July 1989, 353 in situ saphenous vein bypass grafts for occlusive or aneurysmal disease were placed in 328 patients. The study included 264 men and 64 women whose ages ranged from 42 to 92 years (mean, 63 years). Indications for bypass grafting included critical limb ischemia (n = 321, 91%), life-style limiting clandication (n = 18, 5%), and popliteal artery aneurysm (n = 14, 4%). In all but 15 limbs the proximal anastomosis was to the common femoral artery. Other sites of vein bypass graft origin included aortofemoral or femoral-femoral prosthetic grafts (n = 5), and ' popliteal (n = 6) or superficial femoral arteries (n = 4). The site of the distal anastomosis was selected based on angiographic criteria of the leastdiseased artery with patency to the ankle or pedal arch. Eleven patients required interposition of reversed saphenous or cephalic vein to replace sclerotic vein segments or obtain sufficient graft length for anastomosis to the outflow artery. Distal anastomosis was to an infrapopliteal artery in 227 limbs, the below-knee popliteal artery in 120 limbs, and an above-knee or isolated popliteal artery segment in 6 limbs. The technique of in situ bypass grafting has not been modified from our previous reports, t'9 The procedure was performed by means of an open technique with exposure of the entire length of saphenous vein. Intraoperative pulsed-Doppler spectral analysis with a high (20 MHz) frequency Doppler flowmeter, routinely used since 1983, and more recently duplex color flow imaging were used to assess technical adequacy of the bypass graft and to define the hemodynamics of graft blood flow. Measurement of blood flow velocity in the in situ venous conduit was performed under basal flow conditions approximately 20 minutes after restoration of graft blood flow. The technique of intraoperative pulsed-Doppler spectral analysis including selection of recording sites in thc ,venous conduit has been previously described. 1,4,1° Intraoperative studies served as a baseline for comparison with postoperative studies obtained from the identical graft segments by use of duplex scanning. Operative arteriography was used to confirm a technically satisfactory distal anastomosis and patent outflow tract. All patients underwent serial noninvasive hemodynamic testing after operation (intervals of 1 and 7 days, 6 weeks, and every 3 months thereafter). Testing methods included measurement of resting limb arterial pressure by the transcutaneous Doppler ultrasonographic flow detection technique and calcu-
In situ saphenous vein graft thrombosis 681
lation of blood flow velocity from above- and belowknee graft segments by means of (1) a transcutaneous, continuous wave Doppler spectral analysis (5 MHz probe frequency, 45 degree Doppler angle to the skin) if the graft was immediately beneath the skin, or (2) duplex scanning when the graft was more deeply positioned in subcutaneous tissue and more accurate Doppler angle assignment was desired. Graft patency was determined by physical examination, decrease in resting ankle systolic blood pressure as calculated by the ankle-brachial systolic pressure index (ABI), and duplex scanning. An interval decrease in ABI greater than 0.2 was used as a criterion for arteriography or duplex scanning to assess graft patency. Since the focus of this report was the management of acutely thrombosed in situ saphenous vein grafts and indirectly the effectiveness of hemodynamic graft surveillance, six patients who came for treatment weeks after graft failure and had not participated in the surveillance protocol or were lost to follow-up were excluded from the study. Also excluded from the analysis were four patients identiffed by hemodynarnic surveillance to have low graft flow (systolic blood flow velocity less than 45 cm/sec) caused by occlusive lesions in the outflow tract not amenable to revision (verified by arteriography). Graft thrombosis in this cohort was expected and occurred at varied time intervals ranging from 3 to 14 months after documentation of the low-flow state. These patients were not considered for reoperation after graft failure, and all required above- or below-knee amputation. We have previously reported our experience with revision of hemodynamically failing but patent in situ bypass grafts identified by duplex scanning and/or arteriography to have a correctable graft stenosis, and this concept is not addressed in this report? RESULTS Perioperative graft thrombosis. Eighteen (5%) of the 353 in situ saphenous vein grafts thrombosed within 30 days of operation. All but one had as outflow an infrapopliteal (posterior tibial, 9; anterior tibial, 4; peroneal, 3) artery or isolated popliteal artery segment. Critical ischemia was the indication for bypass grafting in all patients. Fourteen grafts occluded within 24 hours of the primary operation. The frequency of early graft failure has remained constant over the duration of this series (Fig. 1). The incidence of perioperative graft thrombosis of 8% observed after the first 87 in situ bypasses (years 1981 to 83) was not significant different (p = 0.2, chi square) from the 4% incidence observed after the
Journal of VASCULAR SURGERY
682 Bandyk et al.
No. of grafts 125
III No. ot in situ bypasses N 30-day thrombosis
100 75 50 25 0
81-83
84-85
86-87
88-89
YEAR Fig. 1. Incidence of perioperative (30-day) thrombosis in a consecutive series of 353 in sire saphenous vein arterial bypass grafts performed during a 9-year period (1981 to 89).
Table I. Mechanism of thrombosis, intraoperative graft blood flow velocity, treatment, and outcome of in situ saphenous vein graft failure within 30 days of operation Mechanism of thrombosis
No.
Inadequate outflow
8
Abnormal venous conduit
5
Technical error Anastomoticocclusion
2
Vein-graft torsion Hypercoagulablestate Total
1 ~ 18
Vp* (cm/sec)
38, 18, ND, ND 30 40 26, 30 35 65, 80, 85 33 33 40 72 60, ND
Secondaryprocedure
No. patent
Thrombectomy-4 Graft translocation Sequential bypass No revision-2 Thrombectomy Graft replacement-3 Graft translocation
0 i 1 0 0 3 1
Graft translocation Vein-patch angioplasty Local revision Thrombectomy
1 1 1 _0 9
ND, not determined.
*Vp, maximumsystolicblood flow velocitymeasuredin distal graft segmentat operation.
last 103 procedures (years 1988 to 89). Correlation of the mechanisms of thrombosis with intraoperative graft hemodynamics and outcome of graft revision are summarized in Table I. Overall, patency was restored and limb ischemia was relieved by conduit revision or replacement in 9 of the 18 patients. Assessment of vein bypass hemodynamics was performed at operation in 15 of 18 patients with early graft thrombosis. In 10 bypass grafts, a low blood flow velocity (systolic velocity o f 40 cm/sec or less) was measured in the distal vein graft segment.
Mechanisms of failure o f these low-flow grafts included inadequate outflow (n = 6), technical error (n = 2), and abnormal venous conduit (n = 2). Thrombectomy alone did not restore patency unless the outflow tract was also modified. O f note, only two other grafts with low flow did not thrombose, the low blood flow velocity in these bypass grafts was attributed to large (5 mm or greater) vein di.~ ametcr. Replacement ofthrombosed small (3 mm or less) diameter, or previously vein-patched graft segments
Volume 11 Number 5 May 1990
In situ saphenous vein graft thrombosis 683
Fig. 2. A, Intraoperative arteriogram of an situ saphenous vein bypass to the distal posterior tibial artery (closed arrow). Sclerotic vein segment below the knee revised with vein-patch angioplasty (curved arrow) after pulsed-Doppler spectral analysis identified abnormal flow pattern as a result of platelet aggregation. After revision, low blood flow velocity (Vp = 33 cm/sec) measured in distal graft segment. B, Intraoperative arteriogram of in situ graft after revision by thrombectomy and translocation of the venous conduit to an isolated popliteal artery segment. Reoperation performed within 12 hours of the primary procedure. Blood flow velocity in distal vein graft was 60 cm/sec. Bypass graft remains patent at 3 years, was successful when the prior level of graft blood flow velocity was adequate (greater than 40 cm/sec, antegrade flow throughout pulse cycle). Mechanisms of thrombosis in five grafts with normal intraoperative hemodynamics included abnormal venous conduits (n = 2), graft torsion, and heparin-induced ,platelet aggregation. Reoperation did not restore vein graft patency in both patients with unrecognized coagulopathy. Of note, translocation of the distal anastomosis to a proximal arterial segment (popliteal artery, 2; posterior tibial artery, 1) successfully relieved critical limb ischemia in three patients whose grafts failed because of poor quality vein or anastomotic occlusion (Fig. 2). Graft replacement with a polytetrafluoroethylene (PTFE) prosthesis was necessary in only one patient when repeated thrombec-
tomy failed to restore patency of the venous conduit. Two patients judged to have inadequate outflow to sustain graft patency did not undergo reoperation. Operative (30-day) mortality was 2.5% (eight patients). One patient developed infection involving the venous conduit and necessitated excision of the bypass graft. For the entire series, 342 (97%) of the 353 in situ bypass grafts were patent when the patient died during the postoperative preiod or was discharged from the hospital. Seven of nine patients with early in situ graft failure required above- or below-knee amputaton. Of the nine bypass grafts salvaged by a secondary procedure, three vein grafts, all to an infrapopliteal artery, occluded within i year. Progression of atherosclerosis in the outflow artery was felt to be the mechanism of failure.
yournaiof VASCULAR SURGERY
684 Bandyk et al.
Table II. Graft hemodynamics before thrombosis, mechanism of thrombosis, treatment, and outcome of unexpected in situ saphenous vein graft failure occurring more than 30 days after primary operation Mechanism of thrombosis Low-flow state (Vp less than 45 cm/sec) Known "graft stenosis"
No.
5
Diseased outflow tract Normal graft hemodynamics (Vp greater than 45 cm/sec) -documented within 3 prior months Thromboembolism
2
FaiRed "jump graft" Unknown -documented greater than 3 months prior Probable "graft stenosis" Total
1 1
4
1 14
Secondaryprocedure
No. patent
Thrombolysis/graft revision-2 Thrombolysis/ PTA~- 1 PTFE+, replacement-2 PTFE replacement-2
2 1 2 0
Thrombolysis/Thrombectomy-2 Thrombectomy/ aneurysm repair-2 PTFE replacement PTFE replacement
2 2 1 1
PTFE replacement 12
~PTA, Percutaneous transluminal angioplasty. tPTFE, Polytetrafluoroethylene.
Late graft thrombosis despite hemodynamic surveillance. After discharge from the hospital, 14 (4%) of 340 in situ bypass grafts thrombosed unexpectedly during a follow-up period that ranged from 3 to 92 months. All occlusions occurred within 1 year of the primary operation or a secondary procedure for graft stenosis. Twelve of the failed grafts were anastomosed to an infrapopliteal artery, and two had a below-knee popliteal artery as outflow. Graft hemodynamics before thrombosis, mechanism of thrombosis, treatment, and outcome of these unexpected graft failures are summarized in Table II. Reoperation was successful in relieving limb ischemia in 12 of the 14 patients, although patency of the in sire venous conduit was restored by thrombolysis (intraarterial urokinase infusion) or direct surgical thrombectomy in only six patients. The most common (n = 6) secondary procedure was graft replacement by means of a PTFE prosthesis. In general, if the secondary procedure corrected the mechanism of thrombosis, prolonged graft patency was observed. Prosthetic replacement of two failed in situ grafts with known low flow as a result of diseased outflow tracts did not remain patent, and both patients required below-knee amputation. In contrast, prosthetic replacement of in sire bypass grafts that occluded as a consequence of thromboembolism, known or presumed graft stenosis, or an unknown cause was successful if normal graft hemodynamics, indicative of adequate graft runoff, had been previously documented by noninvasive testing. Two patients who had undergone prior revision
of a "graft stenosis" with normalization of graft hemodynamics (increase in systolic flow velocity to greater than 45 cm/sec, ABI greater than 0.9) developed unexpected graft failure within 9 months, presumably because of a recurrent stenosis of a patch angioplasty and occlusion of a "jump graft" (Fig. 3). Prosthetic graft replacement was successful in relieving ischemia in both patients. Hemodynamic studies of the 5 or 6 m m diameter PTFE replacement grafts demonstrated a blood flow velocity in the range of 40 to 65 cm/sec. During follow-up, three PTFE replacement grafts failed at postoperative time intervals of 6 weeks, 9 and 14 months. The PTFE graft that failed at 6 weeks had a flow velocity of 40 cm/sec and thrombosed 2 weeks after discontinuation of oral anticoagulation (sodiuna warfarin) because of gastrointestinal bleeding from esophagitis. Two of six veingrafts that underwent thrombolysis/thrombectomy alone or in combination with autologous vein revision thrombosed at 6 and 24 months. Overall, 7 of 14 patients operated on for unexpected graft ~rombosis have maintained patency of the arterial bypass graft with follow-up ranging from 9 to 36 months.. (mean 14 months). DISCUSSION These results confirm in situ saphenous vein bypass grafts that occlude after operation can be treated effectively by reoperation. Limb ischemia was re-lieved in 21 (66%) of a2 patients by a variety of secondary procedures including thrombolysis or thrombectomy, revision with autologous vein, or
Volume 11 Number 5 May 1990
In situ saphenous vein graft thrombosis 685
Fig. 3. (Left) Normal intraoperative arteriogram of femoral-anterior tibial in sire saphenous vein bypass graft. Blood flow velocity in the distal vein graft of 55 cm/sec in normal range. (Middle) Arteriogram obtained 10 days after surgery demonstrated antegrade occlusion of the distal anastomosis (arrow). Low (35 cm/sec) blood flow velocity in distal graft prompted "jump graft" revision to dorsalis pedis artery: (Right) Normal intraoperative arteriogram of femoropopliteal PTFE bypass graft (curved arrow) performed for unexpected in sire thrombosis occurring 2 weeks after discharge from the hospital. Systolic blood flow velocity of 45 cm/sec in PTFE conduit. Graft remains patent at 12 months. prosthetic replacement. If the reoperation corrected .the underlying mechanism of graft thrombosis, was appropriately performed, and restored a bypass graft with normal hemodynamics, long-term patency resulted. Decision making regarding the mechanism of graft thrombosis and thus which restorative procedure, if any, was best suited for each patient was facilitated by prior evaluation of graft hemodynamics. Thrombectomy alone did not restore graft patency when the mechanism of thrombosis was (1) an abnormal venous conduit with traumatized, thrombogenic luminal surfaces or (2) low flow as a result of diseased outflow arteries. In these circumstances the abnormal venous segment should be replaced, preferably with autologous vein, and arterial anatomy of the limb should be reviewed for alternative or additional outflow sites of the bypass graft. An operative strategy that involves modification of the graft runoff when a low-flow state in the graft is documented rather than relying on thrombectomy alone should improve the outcome of graft revision after unexpected thrombosis. Perioperative graft thrombosis is always an usa-
expected complication and as such provokes consternation and dismay in both the patient and surgeon. In a recent report of 1000 consecutive in situ saphenous vein bypass graftings, Leather et al. ~1 reported the incidence of pcrioperative thrombosis was 4.4% for grafts to the below-knee popliteal artery, 3.4% for grafts to the proximal tibial arteries, and 7.8% when grafts are anastomosed to a distal tibial artery. Our experience also confirmed thrombosis of an in situ bypass graft within 30 days of operation was uncommon (incidence, 5%), but we found the incidence of perioperative thrombosis was less (p < 0.02, chi square = 6.5) for[grafts anastomosed the below-knee popliteal artery (0.8%, 1 of 120) compared to infrapopliteal vein bypass grafts (7%, 16 of 227). Our results support the use of intraoperative Doppler ultrasound to confirm technical adequacy and sufficient graft blood flow to strstain patency, and provide further evidence that quality of the venous conduit and status of the outflow tract are important elements in the mechanisms of vein graft failure. Using pulsed Doppler spectral analysis and more recently duplex color flow imaging at opera-
686 Bandyk e~ aI.
tion, we have identified residual lesions (intact valve cusps, anastomotic stricture, platelet aggregation in the venous conduit) that warranted correction in approximately 5% of cases) Duplex color flow imaging has the advantage of allowing assessment of blood flow patterns along the entire length of the reconstruction. This capability facilitates intraoperative assessment and should prove to be useful in evaluating the adequacy of a small (
