Endovascular repair of TAAA results in significant leukocytosis and thrombocytopenia, which appear to be related to postoperative acute renal insufficiency. The inflammatory sequelae may not amount to much after endovascular AAA
repair, but they constitute a significant source of morbidity after endovascular TAAA
repair. In our previous report on the results of multi-branched endovascular TAAA repair, the hemorrhagic complications of thrombocytopenia and coagulopathy included upper gastrointestinal bleeding, hemoptysis, and subarachnoid hemorrhage.5
Based on the findings of the current study, we can conclude that the inflammatory response to endovascular TAAA repair is also associated with renal dysfunction.
The literature on the post-implantation syndrome
following AAA repair provides little indication of the underlying cause. One cannot say, based on published reports, whether the response to endovascular AAA repair is the same as the response to open surgery.10-13
Nor can one say whether the cause is surgical stress, endovascular instrumentation of the mural thrombus, endovascular instrumentation of the endothelium, the presence of a stent- graft, or thrombosis of the aneurysm. For example, some authors suggest that manipulation in the aneurysm during endovascular repair may cause white cell activation with the release of various cytokines, such as IL-1, IL-6, and TNF-α, while others suggest that injury to the vascular endothelium may prompt activation of protein C, with a subsequent coagulopathy and loss of cytoprotectivity.13-14, 17-18
Our data on endovascular TAAA repair are helpful in this regard because the inflammatory response is pronounced and consistent, occurring in every single patient treated. Moreover, there were strong correlations between inflammatory, hematologic and renal effects, suggesting that causal relationships connect them all, although we cannot yet say how. All patients in our study had markedly elevated levels of IL-6 and a two-fold increase in WBC after stent-graft implantation, suggesting a strong inflammatory response. In addition, the coagulopathic response was characterized by a decrease in protein C levels immediately after endovascular repair, followed by a significant drop in platelet count and increase in prothrombin time.
It seems likely that the inflammatory response caused the renal dysfunction, rather than the converse. Other possible explanations for a high rate of postoperative renal dysfunction in this study group include contrast nephrotoxicity and intraoperative ischemia. All of the patients in this study received Visipaque contrast. The mean contrast volume used during repair was 170 mL, with a range of 28 to 390 mL. Of note, the only patient who left the hospital on dialysis was the one who received the smallest dye load (28 mL). There is no period of obligatory renal ischemia during endovascular TAAA repair. Blood flows through the cuffs of the stent-graft into the peri-graft space, and from there into the renal and visceral arteries. In theory, the interruption of flow to a branch vessel would only be occluded for as long as it took to deploy the Fluency covered stent, or to inflate a balloon within the covered stent or the outflow artery. Based on the tapered shape of the stent-graft and the method of insertion, we believe renal ischemia occurred rarely, if ever.
We recognize that alterations in serum creatinine are not necessarily the most reliable basis for an assessment of renal function. In the latter part of this study, we started to measure novel biomarkers of renal function (cystatin C) and renal tubular injury (NGAL).19-20
Cystatin C has emerged as an important marker of acute renal dysfunction, and appears to correlate better with GFR than serum creatinine.21-24
NGAL, an indicator of acute tubular injury, may also have a role in establishing the precise timing of renal injury25
, as we try to establish a chain of events in the interplay of the inflammatory, coagulopathic, and renal effects.
Most of the theories regarding the etiology of the post-implantation syndrome fall into one of two groups: those that depend on catheter-mediated injury, and those that depend on the presence of the stent graft. Since the implantation of a branched stent graft consists largely of a series of intra-arterial catheter manipulations, the duration of the operation may serve a surrogate for the extent of aortic instrumentation. Our surrogates for aneurysm and stent-graft related effects were the extent of aortic coverage and aneurysm diameter. None of these factors correlated with the inflammatory response. The only significant determinant of the extent of the inflammatory response was statin use, with a significantly less pronounced leukocytosis in those taking any form of statin therapy. If anyone needs yet another reason to promote routine statin use in vascular surgery patients, here it is.
The results of endovascular TAAA repair compare well with the results of open surgical repair, but the outcomes are marred by the effects of a severe inflammatory response.5
Not that this response is unique to endovascular repair of TAAA; some manifestations of the post-implantation syndrome
occur in all patients who undergo endovascular treatment of aortic diseases (abdominal aortic aneurysms, thoracic aneurysms, and thoracic dissections).9,13,26-28
However, those undergoing endovascular TAAA repair appear to experience a more extreme response. As we have learned to overcome the technical obstacles to stent-graft insertion, the post-implantation syndrome
has become the main impediment to an uncomplicated postoperative course.