The reported incidence of PIS in the literature varies widely, and the lack of a universally accepted definition may be responsible for this. All patients showed leukocytosis range from 9. However, the cutoffs of these criteria are not specified. Indeed, in eight patients, CT revealed air within the native aorta, around the stent-graft and within the thrombus of the excluded aneurysm. Physical examination, chest radiograph, urinalysis, urine culture and blood culture excluded any source of infection in 11 of 12 patients [ 2 ].
They found that peak values of sedimentation velocity, CRP and interleukin-6 were observed at 7 postoperative days, elevation of leukocytes count occurred in premature phase, while lymphocyte and platelet count occurred in a late phase of follow-up. Once again, neither the definition nor the incidence was stated. However, the definition of PIS is unclear.convecon.xtage.com.br/12325-baile-en-linia.php
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Two other studies described PIS incidence, but they did not clarify the definition used. However, they do not specify the definition that they used. Several studies defined PIS as a combination of two criteria: leukocytosis and fever. PIS occurred in 49 patients In this study, the authors did not characterize the population in detail and opted to describe consequences of PIS in six cases.
In this way, they compared the group in which the patients go home in the same-day of the procedure to the non-ambulatory-group and evaluate the incidence of PIS in these two groups.
In another study, with a retrospective design, of patients who underwent EVAR but only with Anaconda endograft. They also used the same criteria described above for PIS.
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They found an incidence of PIS of PIS was diagnosed in A German group studied the effects of antibiotics in preventing PIS after aortic endoprosthesis implant. This trial included 40 patients and they did not have an aneurysmal disease. In each group, there were 18 type B dissections and 2 penetrating aortic ulcers. There were no differences in parameters related to PIS, namely body temperature, leukocytes count and CRP, between two groups. They also did not find differences between the groups of acute and chronic type B dissections [ 23 ].
This inflammatory response after TEVAR was associated to a rise in body temperature in the postprocedure period. In conclusion, many studies do not specify the PIS definitions, many others used the definition with leukocytosis and fever and only three studies used a definition that includes CRP. The reported incidences in literature vary greatly which is possibly a consequence of variability in definitions. Hence, the obvious need for a universal definition of this syndrome. Implant composition has been identified as one of the most important determinants of the incidence and severity of PIS.
So, factors other than implant material must also be responsible to the occurrence of PIS. These may be patient or implant related.
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This is the best investigated risk factor; several studies compared the incidence of PIS or the difference in inflammatory parameters and endograft material, mainly focusing on differences between polyester and expanded politetrafluoroethylene ePTFE -based structures. The majority of the studies pointed to a higher incidence of PIS or a greater increase of inflammatory markers in polyester-based endografts [ 4 , 5 , 8 , 18 , 20 ]. Despite the results, another three studies could not identify a difference in the incidence of PIS between polyester and ePTFE endografts.
However, there were no statistically significant differences between two groups, for all endpoints, possibly due to sample size. It could also be related to sample size, with 32 patients treated with polyester grafts but only 13 patients with ePTFE grafts. They performed a sensitivity analysis that showed if three more patients in the polyester group would have developed PIS or none instead of one patient in the PTFE group , the results would have reached significance.
They attributed that to small number of patients implanted with ePTFE endografts in their trial. Apart from fabric, other components of the graft structure could be implicated.
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The stent structure, for example, could influence the occurrence of PIS. Moreover, the latter have a bare top stent which constitutes an additional amount of nitinol directly exposed to the circulation and to the vessel wall. In addition to amount of alloy exposition, the exact balance between nickel and titanium components of nitinol or even the way of cutting and polishing may differ between manufacturers and may influence the inflammatory reaction [ 5 ].
Delivery systems could also theoretically influence PIS. They hypothesize that this may cause less injury to endothelium. Moreover, thickness and porosity may differ between polyester endografts, as the metallic skeleton, and can justify variability in inflammatory response after EVAR [ 25 ]. Despite all the proposed mechanisms, the only component of endografts that seems to influence the incidence of PIS significantly is the fabric.
The hypothesis that the amount of preexisting mural thrombus within the aneurysm sac could be related to PIS development derived from the finding that mural thrombus of an aortic aneurysm contains high levels of interleucin-6 [ 29 ]. In this way, it was conjectured that manipulations with endovascular material, as wires and catheters, in mural thrombus could release interleucin-6 and induce an inflammatory response. Another hypothesis was that new-onset thrombus, instead of chronic mural thrombus, could be responsible for the acute inflammatory response [ 30 ].
Three authors tried to demonstrate this effect of new-onset thrombus but the results were not consistent. In a multiple variable model, these authors showed that both the volume of new-onset thrombus and the type of endograft were independently associated with the development of PIS. In light of the current evidence, it is not likely that chronic mural thrombus or new-onset thrombus within the aneurysm sac play a significant role in the development of PIS. It is possible that new onset thrombus may play a small role, which could not yet be clearly demonstrated due to sample size in all published studies on the subject.
Another potential etiology for PIS after endovascular aneurysm repair is bacterial translocation due to transient sigmoid ischemia. Intestinal ischemia may be produced by either occlusion of a previously patent inferior mesenteric artery IMA or microembolization during catheter and wire manipulations. Another trial, that studied the effects of antibiotic therapy in PIS after thoracic aortic stent placement, is in agreement [ 23 ].
The authors stated that there were no differences in parameters related to PIS, regardless of the duration of postoperative antibiotic therapy. Therefore, the hypothesis of bacterial translocation as a cause for PIS seems remote and there is no evidence to date to support it.
There are other recent studies that specifically analyzed inflammatory response after endovascular aortic repair; however, they did not find any correlation between contrast use or dosage and PIS parameters [ 5 , 8 , 18 , 25 ]. As such, this theory remains to be demonstrated. The influence of several other factors in PIS parameters has also been explored, namely age, gender, aneurysm size, extent of aortic coverage, length of operation, blood loss or transfusion, intensive care unit, statin, chronic obstructive disease, ischemic heart disease and heart failure.
None has been shown to be an important factor to PIS [ 5 , 8 , 9 , 14 , 18 ]. The diagnosis might be suspected in the presence of fever without clinical source of infection in the immediate postoperative period after EVAR. However, the diagnosis of PIS will depend on definition that is adopted. Fever is usually accompanied by a rise in laboratorial inflammatory markers and a drop in platelet count.
Leukocytes count typically rises in the first postoperative day [ 5 , 25 ]. In the presence of fever and inflammatory parameters in the early postoperative period, patients usually undergo a work-up for possible infection, typically including chest radiography, urinalysis, urine culture and blood culture [ 32 ]. Some argue that this may be costly and unnecessary in clinical absence of an infection source [ 33 ].
However, since consequences of a serious postoperative infection may be devastating, at least close observation is recommended. The global incidence of PIS in this trial was Thus, procalcitonin appears as a good differentiator between PIS and infectious complications, probably less expensive and faster than microbiologic culture tests.
Summary table of the studies that favor influence of PIS in outcomes and of those that are against. Other studies showed a significant prolongation of postoperative hospitalization in the PIS group compared to non-PIS group [ 4 , 10 , 20 ]. In a study concerning the applicability of percutaneous ambulatory EVAR, one patient was also readmitted due to severe PIS in third postoperative day in the non-ambulatory group and PIS was the only reason for delayed discharge in five patients [ 6 ].
These authors found that patients with postoperative renal insufficiency had higher changes in leukocytes and platelets counts, as compared with those who did not develop renal failure. Indeed, the two patients who died in first postoperative month developed acute renal insufficiency in the early postoperative period.
Biomechanical and histologic analysis in aortic endoprosthesis using fibrin glue. Alternatives have been tested aiming to improve this incorporation. Fibrin glue is used in many operating procedures promoting adhesion and tissue regeneration; however, its use to improve EP incorporation by arteries is unknown. View on PubMed. Open Access. Save to Library. Create Alert.
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References Publications referenced by this paper. Distal migration of stent-grafts after endovascular repair of abdominal aortic aneurysms. Nitrogen-rich coatings for promoting healing around stent-grafts after endovascular aneurysm repair. Blood flow and structure interactions in a stented abdominal aortic aneurysm model. Zhonghua Li , Clement Kleinstreuer. Mathematical Model analysis of Wallstent and Aneurx: dynamic responses of bare-metal endoprosthesis compared with those of stent-graft.
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