Evaluating proximal clamp site and intraoperative ischemia time among open repair of juxtarenal aneurysms.

BACKGROUND: The proportion of open aneurysm repairs requiring at least a suprarenal clamp has increased in the past few decades, partly owing to preferred endovascular approaches for most patients with infrarenal aneurysms, suggesting that the management of aortic clamp placement has become even more relevant. This study evaluated the association between the proximal clamp site and intraoperative ischemia times with postoperative renal dysfunction and mortality. METHODS: We used the Vascular Quality Initiative to identify all patients undergoing open repairs of elective or symptomatic juxtarenal AAAs from 2004 to 2018 and compared outcomes by clamp site: above one renal artery, above both renal arteries (suprarenal), or above the celiac trunk (supraceliac). Outcomes evaluated included acute kidney injury (AKI), new-onset renal failure requiring renal replacement therapy (RRT), 30-day mortality, and 1-year mortality. We used multilevel logistic regressions and Cox proportional hazards models, clustered at the hospital level, to adjust for confounding. RESULTS: We identified 3976 patients (median age, 71 years; 70% male; 8.2% non-Caucasian), with a median aneurysm diameter of 5.9cm (interquartile range [IQR], 5.4-6.8 cm). Proximal clamp sites were above one renal artery (31%), suprarenal (52%), or supraceliac (17%). The rates of unadjusted outcomes were 20.5% for AKI, 4.1% for new-onset RRT, 4.9% for 30-day mortality, and 8.3% for 1-year mortality. On adjusted analyses, independent of ischemia time, suprarenal clamping relative to clamping above a single renal artery had higher odds of postoperative AKI (adjusted odds ratio [aOR], 1.50; 95% confidence interval; 95% CI, CI, 1.28-1.75), but similar odds for new-onset RRT (aOR, 1.27; 95% CI, 0.79-2.06) and 30-day mortality (aOR, 1.12; 95% CI, 0.79-1.58) and hazards for 1-year mortality (adjusted hazard ratio, 1.12; 95% CI, 0.86-1.45). However, every 10 minutes of prolonged intraoperative ischemia time was associated with an increase in odds or hazards ratio of postoperative AKI by 7% (IQR, 3%-11%), new-onset RRT by 11% (IQR, 4%-17%), 30-day mortality by 11% (IQR, 6%-17%), and 1-year mortality by 7% (IQR, 2%-13%). Patients with more than 40 minutes of ischemia time had notably higher rates of all four outcomes. CONCLUSIONS: Suprarenal clamping relative to clamping above a single renal artery was associated with AKI, but not new-onset RRT or 30-day mortality. However, the intraoperative renal ischemia time was independently associated with all four postoperative outcomes. Although further studies are warranted, our findings suggest that an expeditious proximal anastomosis creation is more important than trying to maintain clamp position below one renal artery, suggesting that suprarenal clamping may be the best strategy for open AAA repair when needed to efficiently perform the proximal anastomosis.

Factors associated with postoperative renal dysfunction and the subsequent impact on survival after open juxtarenal abdominal aortic aneurysm repair.

BACKGROUND: Renal dysfunction is a well-described complication of open juxtarenal abdominal aortic aneurysm repair, but the associated risk factors and corresponding impact on survival are not well described. METHODS: We identified all patients not on hemodialysis undergoing open repair of nonruptured juxtarenal aneurysms in the Vascular Quality Initiative from 2003 to 2017. We used mixed-effects logistic regression to determine factors associated with in-hospital postoperative renal dysfunction, including acute kidney injury (AKI, defined as serum creatinine concentration increase >0.5 mg/dL) and new renal replacement therapy (RRT), as well as the association between postoperative renal function and perioperative mortality. Cox regression was used to determine the association between postoperative renal complications and long-term survival. RESULTS: We identified 2635 open juxtarenal repairs, of which 621 (24%) were complicated by AKI. The majority of these (20% of the overall cohort) were AKI alone, but 2.2% required temporary RRT and an additional 1.7% were permanently dialysis dependent. Factors independently associated with postoperative renal dysfunction included renal-visceral ischemia time (per minute: odds ratio [OR], 1.01 [1.01-1.02]; P < .001), clamp site (above both renal arteries: OR, 1.4 [1.1-1.8; P = .02]; supraceliac: OR, 1.7 [1.1-2.5; P = .01]), statin use (OR, 1.5 [1.1-2.0]; P = .01), male sex (OR, 1.7 [1.2-2.2]; P = .002), and preoperative renal function (glomerular filtration rate [GFR] of 45-60 mL/min/1.73 m2: OR, 1.8 [1.3-2.5; P < .001]; GFR of 30-45 mL/min/1.73 m2: OR, 1.9 [1.2-2.8; P = .003]; GFR of <30 mL/min/1.73 m2: OR, 6.2 [3.1-12.2; P < .001]). When renal-visceral ischemia time was categorized, there was no difference in risk of postoperative renal dysfunction until >25 minutes, but risk increased stepwise thereafter (25-39 minutes: OR, 1.6 [1.2-2.1; P = .004]; 40+ minutes: OR, 2.6 [1.9-3.5; P < .001]). Neither mannitol nor the use of cold renal perfusion was associated with renal complications or mortality in the overall cohort, but cold renal perfusion was associated with lower risk of AKI when clamp times exceeded 25 minutes (OR, 0.4 [0.2-0.97]; P = .041). Postoperative renal dysfunction was associated with higher adjusted perioperative mortality (AKI: OR, 2.6 [1.4-5.0; P < .01]; RRT: OR, 10.5 [4.0-27.6; P < .001]) and significantly higher risk of long-term mortality (AKI: hazard ratio, 1.5 [1.0-2.1; P = .049]; RRT: hazard ratio, 5.8 [3.2-10.3; P < .001]). CONCLUSIONS: Postoperative renal dysfunction, even a mild elevation in creatinine concentration, is associated with higher perioperative and long-term mortality. Although the routine use of mannitol and cold renal perfusion was not associated with postoperative renal dysfunction after open juxtarenal repair, cold renal perfusion was associated with lower risk of AKI if clamp times exceeded 25 minutes.

Severe contralateral carotid stenosis or occlusion does not have an impact on risk of ipsilateral stroke after carotid endarterectomy.

OBJECTIVE: This study evaluates the impact of severe (>70%) contralateral carotid stenosis or occlusion (SCSO) on outcomes after carotid endarterectomy (CEA). METHODS: Clinical data for all patients undergoing CEA at a single center were prospectively gathered and retrospectively reviewed, with the sample population stratified according to the presence of SCSO. Perioperative outcomes of CEA in the presence of SCSO were analyzed using univariate and multivariate methods. RESULTS: During a 17-year study period, 2945 CEAs were performed on 1843 patients, including 736 (25%) patients with SCSO. Patients identified with SCSO had a higher rate of positive intraoperative electroencephalographic changes (30% vs 16%; P < .0001) and use of an intraoperative shunt (40% vs 28%; P < .0001). Univariate analysis identified SCSO as a risk factor for any stroke (2.8% vs 1.5%; P = .02), death (2.2% vs 1.1%; P = .02), and any stroke/death (4.3% vs 2.4%; P < .0079) but not ipsilateral stroke (1.5% vs 1.2%; P = .38). Multivariable regression demonstrated SCSO as an independent predictor of any stroke (odds ratio [OR], 1.8; 95% confidence interval [CI], 1.0-3.3; P = .05) and any stroke/death (OR, 1.7; 95% CI, 1.1-2.7; P = .02), without increasing risk of ipsilateral stroke (OR, 1.3; 95% CI, 0.6-2.7; P = .54). The presence of SCSO was also associated with a higher risk of late mortality (hazard ratio, 1.3; 95% CI, 1.1-1.4; P < .01). CONCLUSIONS: Although the presence of SCSO is a risk factor for any stroke/death with CEA, it does not increase the risk of ipsilateral stroke. These data suggest that increased attention to perioperative medical and hemodynamic management should be especially considered in this cohort of patients as the observed strokes do not occur in the territory at risk from the surgical procedure.

Endovascular management of axillo-subclavian arterial injury: a review of published experience.

BACKGROUND: The role of endovascular treatment for vascular trauma, including injury to the subclavian and axillary arteries, continues to evolve. Despite growing experience with the utilization of these techniques in the setting of artherosclerotic and aneurysmal disease, published reports in traumatic subclavian and axillary arterial injuries remain confined to sporadic case reports and case series. METHODS: We conducted a review of the medical literature from 1990 to 2012 using Pubmed and OVID Medline databases to search for all reports documenting the use of endovascular stenting for the treatment of subclavian or axillary artery injuries. Thirty-two published reports were identified. Individual manuscripts were analysed to abstract data regarding mechanism, location and type of injury, endovascular technique and endograft type utilized, follow-up, and radiographic and clinical outcomes. RESULTS: The use of endovascular stenting for the treatment of subclavian (150) or axillary (10) artery injuries was adequately described for only 160 patients from 1996 to the present. Endovascular treatment was employed after penetrating injury (56.3%; 29 GSW; 61 SW), blunt trauma (21.3%), iatrogenic catheter-related injury (21.8%) and surgical injury (0.6%). Injuries treated included pseudoaneurysm (77), AV fistula (27), occlusion (16), transection (8), perforation (22), dissection (6), or other injuries otherwise not fully described (4). Initial endovascular stent placement was successful in 96.9% of patients. Radiographic and clinical follow-up periods ranging from hospital discharge to 70 months revealed a follow-up patency of 84.4%. No mortalities related to endovascular intervention were reported. New neurologic deficits after the use of endovascular modalities were reported in only one patient. CONCLUSION: Endovascular treatment of traumatic subclavian and axillary artery injuries continues to evolve. Early results are promising, but experience with this modality and data on late follow-up remain limited. Additional multicenter prospective study and capture of data for these patients is warranted to further define the role of this treatment modality in the setting of trauma.

Luminal thrombus disrupts nitric oxide-dependent endothelial physiology.

BACKGROUND: The goals of this study were: (1) to develop a large animal model to study endothelial function, and (2) to determine if arterial thrombosis induces endothelial dysfunction in vivo. METHODS: Surgical exposure of the porcine iliac and femoral arteries was performed. Normal porcine arteries were compared with arteries subjected to 90 min of arterial thrombosis. External iliac artery (EIA) luminal diameters were measured using M- and B-mode duplex ultrasound. Endothelium-dependent relaxation (EDR) and endothelium-independent relaxation (EIR) were measured using acetylcholine (ACh) and sodium nitroprusside (NTP), respectively. Endothelial integrity was determined by factor VIII immunohistochemistry (F8) and scanning electron microscopy (SEM). Nitric oxide levels were determined using a chemiluminescence assay of nitrite/nitrate metabolites (NO(x)). Continuous variables were analyzed using the two-tailed Student t test. RESULTS: Control artery EDR was 80 +/- 7.1% (+/- SE), while arteries exposed to luminal thrombus for 90 min had an EDR of 55.2 +/- 5.7% (ACh = 15 microg/min, n = 11, P = 0.0231). EIR was preserved in normal and thrombosis groups with uniform response to NTP (4.92 +/- 0.1 cm vs 5.07 +/- 0.42 cm, P = 0.76). F8 staining identified endothelium in all groups. SEM analysis revealed an intact monolayer of endothelium after thrombosis. Local NO(x) levels were 17.3% lower after 90 min of thrombosis (49.3 microM vs 40.8 microM, n = 16, P < 0.001). CONCLUSIONS: Luminal thrombus induces arterial dysfunction acutely without causing endothelial cell loss. EIR remains unaffected, indicating normal smooth muscle cell function. NO(x) levels suggest that nitric oxide levels are decreased acutely after thrombosis. The development of this porcine large animal model allows the in vivo study of vasospasm and alternative thrombolytic regimens.