Endovascular aneurysm repair currently has a limited role for the treatment of aortic disease around the visceral-renal arteries. Therefore, OAS is still the gold standard treatment for patients with para-renal or para-visceral aortic disease. OAS is also challenging because it requires more extensive surgical exposure, has an increased risk of ischemic injury to renal and visceral organs or the spinal cord, and increased cardiac and pulmonary demands during SRACC. Therefore, OAS requiring SRACC carries a higher morbidity and mortality than infra-renal aortic surgery.
Greenberg et al. [12
] recently reported excellent treatment results in patients with JRAA or TAAA using branched aortic stent grafts. However, the use of these devices is still not allowed in Korean or even in the United States, except in clinical trials. The results achieved by a few specialized centers cannot be generalized. As an alternative method to branched aortic stent grafting, aortic stent grafting with viscera and/or renal revascularization with a chimney technique can be used for the treatment of para-renal aortic aneurysms [13
]. However, it remains to be determined whether the long-term results of the chimney procedure are equivalent to those of branched aortic stent grafting or OAS.
Since endovascular treatment for AAA and AOD are being more frequently performed, a greater proportion of OASs have become more complex [14
]. Though the frequency of OAS requiring SRACC varies from center to center, it has a referral pattern to large centers. During the study period, 14% of patients undergoing OAS required SRACC in our hospital.
Some may argue against including type IV TAAA as an AAA. Though it is classified as a type of TAAA, it is apparent that type IV TAAA does not affect the thoracic aorta, but it does affect the abdominal aorta. Therefore, we included type IV TAAA as an AAA requiring SRACC.
Renal insufficiency is one of the most serious complications after SRACC. The reported incidence of PORI after OAS requiring SRACC ranges from 7.9 to 38%, which depends on the definition of PORI [15
]. In this study, 21% (14/66) of patients developed PORI, which was defined as sCr elevated greater than 50% over the preoperative level. New HD was required in 4 (6%) of these patients; however most required temporary HD, while one patient (1.5%) who developed chronic renal failure required chronic HD. That patient presented with ruptured type IV TAAA and preexisting renal insufficiency. Numerous authors have reported that PORI develops more often in females, and patients with preoperative renal insufficiency, intraoperative hypotension, concomitant renal artery reconstruction and prolonged RIT [17
]. In the present study, SCACC and RIT ≥25 minutes were identified as risk factors of PORI on univariate analysis.
The optimal site of aortic cross clamping is usually determined by the extension of the aortic lesion, associated arterial disease requiring concomitant repair, body habitus, etc. Green et al. [21
] reported that SCACC carries a lower risk of PORI than aortic clamping just proximal to the renal arteries, which can prevent atheroembolism from the para-renal aortic lesion. Shortell et al. [17
] also reported the merit of SCACC in patients with JRAA, including a reduced incidence of complications related to proximal aortic cuff disease. However, many previous authors have reported that SCACC is an independent predictor of PORI [20
]. At our institution, we prefer aortic clamping at the inter-renal or supra-renal aorta to supra-celiac aorta, unless there is significant aortic calcification or mural thrombus around the renal artery orifices.
In addition to atheroembolism, acute tubular necrosis due to interruption of renal perfusion is a well-known pathogenesis of PORI. In an experimental rat model of renal ischemia, renal blood flow to the outer medullary area decreased dramatically during the first 30 minutes of renal ischemia and showed transient recovery to 50% of baseline blood flow for a three-hour period [23
]. Prolonged RIT is a well-known independent risk factor for PORI. However, tolerable time duration to irreversible damage of the renal tissue was not well established after renal perfusion was stopped. Wahlberg et al. [18
] reported the frequency of PORI according to the total RIT. According to them, PORI was very rare when the RIT was shorter than 25 minutes. The odds ratio increased to 2.2 (95% confidence interval [CI], 0.5 to 8.8) and 12 (95% CI, 1.0 to 141.3) when RIT lasted 26 to 50 minutes and >50 minutes, respectively. In the present study, RIT >25 minutes was a significant predictor of PORI on univariate analysis, but not on multivariate analysis.
Various protective measures and adjunctive surgical procedures are performed to reduce renal or visceral ischemic injury in patients with supra-renal or type IV TAAA. Though Cochrane Collaboration [24
] recently reported that there is insufficient evidence to support the routine use of renal protective measures during aortic surgery, renal parenchymal cooling by the infusion of cold solution into the renal artery and prophylactic intravenous administration of mannitol and/or furosemide are frequently used to reduce renal ischemic injury. Our policy is to administer mannitol and furosemide intravenously before SRACC, and to infuse cold heparinized solution into the renal artery when prolonged RIT is anticipated. A typical example is cooling of the left kidney when a separate left renal artery reconstruction is planned after the completion of proximal aortic anastomosis. According to Knott et al. [19
], 12% of juxta-renal AAA patients required renal artery revascularization during OAS. In the present series, renal artery revascularization was performed in 29% of patients who required suprarenal aortic clamping during OAS. These findings are similar to those of Chong et al. [7
] who found the frequency of concomitant renal artery revascularization was 32% in patients who underwent OAS requiring SRACC.
SCACC is required in cases of type IV TAAA and some cases of suprarenal AAA. The amount of blood flow to the gastrointestinal tract, splanchnic organs and both kidneys is known to account for 55% of cardiac output [25
]. Therefore, SCACC causes an increased cardiac afterload in addition to the renal, splanchnic and lower extremity ischemia. Major adverse effects can occur with SCACC, resulting in ischemia-reperfusion injury of the visceral organs. One of the most dreaded complications after prolonged SCACC is the development of intraoperative bleeding. Anagnostopoulos et al. [26
] described the mechanisms underlying intraoperative bleeding tendency in an animal model that underwent SCACC for longer than 30 minutes. They explained that these mechanisms involved systemic intravascular thrombosis resulting in consumption coagulopathy and decreased fibrinolytic activity ("fibrinolytic shutdown") following ischemia-reperfusion of visceral organs. Hepatic hypoperfusion can cause decreased clearance of tissue plasminogen activator (t-PA) in the liver while increased t-PA production by the ischemic gut. Nypaver et al. [27
] reported that postoperative complications related to organ ischemia developed in 14% of patients who underwent SCACC longer than 45 minutes during an elective OAS concomitant with renal or visceral artery revascularization.
Acute pancreatitis is a very rare complication after OAS [28
]. The possible mechanisms of acute pancreatitis after SCACC include systemic or regional hypoperfusion of the pancreas, atheroembolism of the arteries supplying the pancreas, and mechanical injury to the pancreas. However, clinical features of postoperative pancreatitis can be obscured due to abdominal wound pain and gastrointestinal dysfunction in the immediate postoperative period. When we adopted the elevation of serum pancreatic enzymes by three times or more compared to the preoperative level as the definition of postoperative pancreatitis, the incidence was very rare after SCACC. Though SCACC can cause visceral organ ischemia, morbidity due to splanchnic organ hypoperfusion is often reported to be minimal [29
]. Elevation of pancreatic and/or hepatic enzymes was observed after SCACC, but most returned to normal levels within two weeks.
To summarize our observations, OAS requiring SRACC or SCACC can result in renal or visceral complications. However, if the RIT is shorter than 25 minutes, SRACC is considered a safe procedure. Though we were unable to identify independent risk factors for PORI, we found that preexisting renal disease can progress to chronic renal failure after SRACC. We have encountered good short-term and long-term results after OAS with supra-renal or SCACC.