- Review Article
- Open Access
- Published:
Endotension: twenty years of a controversial term
CVIR Endovascular volume 4, Article number: 46 (2021)
Abstract
Use of the term endotension in the treatment of aortic aneurysm is currently controversial. Initially it was proposed to define the circumstance in which there is an enlargement of the aneurysm sac after endovascular repair without a demonstrable endoleak. The term was established with the aim of transmitting the possibility of causes other than pressure applying stress to the aneurysm wall. Twenty years have passed since the proposal of this terminology was published. The literature is reviewed with the purpose of providing an update on advances in the knowledge of the possible etiological mechanisms. The experimental studies call into question that causes other than pressure determine the increase of the aneurysm. On the basis of this review, the term `Sac Expansion Without Evident Leak´ (SEWEL) is proposed as a more accurate and precise denomination for what is aimed to be defined. Evidence suggests that the more likely mechanisms of persistent pressurization of the aneurysm sac are an unidentified endoleak (likely type I or low-flow Type II) or thrombus occluding wide and short channels that connects with the excluded aneurysm sac (at the attachment sites of the stent-graft or at the branch vessels orifices).
Introduction
The term endotension was firstly proposed by Gilling-Smith et al. They defined endotension as “persistent or recurrent pressurization of aneurysm sac following endovascular repair”. They also established a classification of endotension: Grade I was related to type I endoleak, Grade II to type II endoleak, whereas Grade III was related to pressure transmission through the graft (Gilling-Smith et al. 1999). White GH and May J described this scheme as confusing and they defined endotension as “persistent or recurrent pressurization of an aneurysm sac after endovascular graft implantation, without evidence of endoleak”. In the same article they proposed the classification of endoleaks currently in force. In their own words, the term endotension “nicely implies something related to but distinct from endoleak” whereas “conveys the possibility of causes other than pressure applying stress to the aneurysm wall” (White and May 2000). It is important to highlight that tension has several mechanical or physical interpretations, and not only that referred to a fluid pressure. It also defines the state of being stretched, pulled or twisted, and that is the reason why it was deemed more appropriate than endopressure. Be that as it may, the definition of endotension remains a controversial issue. At present, the strict usage of the term is reserved for those circumstances in which there is an aneurysm sac enlargement without a demonstrable endoleak on a delayed contrast computed tomography (CT) scan or other modalities.
Most of aneurysms shrink in size or remain unchanged after endovascular repair. It is widely assumed that the cause is a decrease of pressure within the aneurysm sac. Chuter et al. demonstrated that sac pressure decreases immediately after endovascular repair with aortomonoiliac stent-grafts (Chuter et al. 1997). Sánchez et al. observed the same finding in a canine model (Sanchez et al. 1997) and Parodi et al. in an experimental model using PTFE stent-grafts (Parodi et al. 2001).
In contrast, some aneurysms increase in size following endovascular repair. In most of them, endoleaks are identified. However, some cases of aneurysm enlargement (White et al. 1999; Lin et al. 2003) and even rupture (Kougias et al. 2008) were reported, in which an associated endoleak was not detected. Several hypotheses were proposed to explain these cases. First, pressure could be transmitted to the sac through arterial wall thrombus lining the attachment site of the endograft or through thrombus “sealing” a type 1 endoleak. The pressure could be also transmitted through thrombus originated over the orifices of aortic or iliac branches of the aneurysm. Secondly, one of the most accepted theories is the limitation of current imaging techniques to detect some endoleaks, particularly if the flow is low. Third, another theory proposed the pressure transmission through the endograft wall in the case that material porosity is high. It may also arise through small defects in the fabric of the graft or because of endograft pulsality. Fourth, a pressure buildup from fluid accumulation within the sac was suggested. Seroma-like fluid could accumulate gradually because of thrombus fibrinolysis, graft infection, enzymatic activity or genetic modulation. One last theory proposed that aneurysm enlargement may be independent of pressure.
Twenty years after the proposal of these hypotheses, we reviewed the literature with the purpose of providing an update on advances in the knowledge of the possible etiological mechanisms. The review of the international literature was performed using Medline. The key words “endotension” and “endotension endoleak” were initially used. We found 138 citations from 1999 to 2020. Studies were included in the review if they were related to the concept and etiopathogenesis of endotension after EVAR. Eighteen articles were initially selected. The search was then extended to related articles suggested by the databases and supplemented with searches of reference lists of all relevant articles.
Review of the literature
Pressure transmission through thrombus
Certain studies support the theory of pressure transmission though a thrombus or a clot. In an experimental study in a canine model, Marty et al. found that in the group of excluded aneurysms without an endoleak, intraaneurysmal pressure ratio showed a decline to a ratio of 0.34 compared to systemic pressure. In the group of aneurysms with an endoleak, pressure ratio stabilized at 0.75 and the aneurysms remained pulsatile, although the pressure pulse was lower (30 mmHg) than that of untreated aneurysms (62 mmHg). After “sealing” of endoleaks by coil embolization (arteriography and computed tomography confirmed the “sealing”), intraaneurysmal pressure ratio did not decrease (0.76) (Marty et al. 1998).
In another ex vivo study, Mehta et al. created endoleak channels of various lengths and diameters using polytetrafluoroethylene (PTFE) grafts. Peak systolic pressure was recorded in the aneurysm sac, distal to each endoleak channel, before and after the channels were filled with human thrombus. In the absence of thrombus the pressure did not change across the channels, regardless of its length or diameter. In contrast, when an endoleak was thrombosed, pressure reduction was directly proportional to the length and inversely proportional to the diameter of its channel. The authors concluded that thrombosis of endoleaks with short and wide channels may not result in substantial pressure reduction within the aneurysm sac and a successful outcome (Mehta et al. 2001).
Pressure transmission through the endograft
In an in vitro experimental study, Gawenda et al. analyzed the pressure transmission through the endoluminal graft to a latex aneurysm connected to a circulation model containing a pulsatile pump and a silicone tubing system (Gawenda et al. 2003). The authors found transmission of pulsatile pressure to the latex aneurysm through the graft and they hypothesized that the reason for this phenomenon was what they named “diaphragm effect”. Three different types of grafts were used: thin-wall PTFE, thick-wall polyethylene and thin-wall polyethylene. The conclusion was that transmitted pressure increased with augmenting systemic pressure and it depends on the graft material. Thus, transmitted pressure with PTFE grafts was significantly lower to that recorded with polyethylene grafts whereas pulsatile pressure was lower with low compliance grafts. One important limitation of this study was that commercially available stent-grafts, provided with a wire mesh to enhance columnar strength and radial fixation, were not included. In another experimental in vitro study, they compared the obtained pressures in aneurysm models with 6 or 12 layers, resulting in elastic and stiff compliance. They concluded that pressures were influenced by the compliance (Gawenda et al. 2004).
In contrast, in a more recent in vitro study in a latex model, Bosman et al. demonstrated that pressure transmission through the commercially available stent-grafts wall is clinically irrelevant (Bosman et al. 2009). Seven types of endografts were used: a 3-layer latex tube as reference, a knitted thick-wall Dacron tube graft, a woven thin-wall Dacron tube graft, a thick-wall expanded PTFE tube graft, an Excluder endoprosthesis (WL Gore & Associates, Flagstaff, AZ, USA), a Zenith stent-graft (Cook, Bjaeverskov, Denmark) and a AneuRx stent-graft (Medtronic Vascular, Santa Rosa, CA, USA). The latex reference was used to see if a very compliant “graft” would cause large pressure increases. The thick-wall and the thin-wall Dacron tube grafts, as well as the thick-wall expanded PTFE tube graft, were based on Gawenda’s research. Testing was conducted in an in-vitro pulsatile flow model that was previously described and validated. The systolic and diastolic intra-aneurysm pressures were measured, along with the pulse pressure. The mean intra-aneurysm pressure and pulse pressures were compared for each category of graft (stented/stentless) and for each graft. They found that with increasing systemic pressures, there was a small pressure increase in the aneurysm (< 5 mmHg). In addition, there was no significant difference among the various types of endografts in the dynamic or the static experiments, whereas the pulse pressures were almost identical for all the grafts, not correlating with the stiffness. Therefore, no significant difference in the pressure transmission between stented and stentless grafts was found. According to this finding, the influence of graft rigidity on endotension and the acclaimed “diaphragm-effect” seem less plausible. This study seriously called this effect into question.
Reliability of imaging methods
In a summary of opinions expressed at an international conference and published in 2002, consensus was reached that some endoleaks could not be detected with even optimal CT scanning. Some authors think that endotension is actually a not identified endoleak by conventional imaging (Lin et al. 2003; Meier et al. 2001; Blackwood et al. 2016). Supporting this theory, there is a reported case of an enlarging aneurysm that was diagnosed as endotension and during open surgery a type III endoleak was demonstrated (Yoshitake et al. 2015).
What seems true is that an ideal imaging technique for endoleak diagnosis is still not available. Duplex ultrasound (DUS), magnetic resonance angiography (MRA), conventional angiography and CT rely on a net movement of fluid or contrast within a certain defined period of time. With each method there is a limit of resolution at which point a small endoleak may remain hidden.
CT has traditionally been considered the gold standard and remains the preferred methodology to evaluate patients. Usually, type I and III endoleaks are detected in arterial phase, whereas type II are detected on a delayed phase. Most CT protocols do not perform delayed imaging with > 180 s postcontrast injection (Rozenblit et al. 2003; Iezzi et al. 2006). However, some studies recommend a delayed CT protocol of up to 300 s to identify low flow endoleaks (Iezzi et al. 2008). Recently, some authors have advocated for using a single-acquisition split-bolus protocol, with simultaneous acquisition of arterial and delayed phase imaging, which could reduce radiation dose by up to 43% (Javor et al. 2017). Photon-counting detector (PCD) CT is an emerging technology, with potential application in EVAR surveillance. The acquisition of CT images at greater than two energy bins allows for better tissue discrimination (Dangelmaier et al. 2018). Improved tissue and material discrimination with PCD CT has potential for both better visualization and dose reduction in the evaluation of endoleaks.
MRA is an alternative, but it requires caution if the stent-graft skeletal is made of steel. Furthermore, the endograft material can influence study quality because stainless steel cause significantly more susceptibility artifact that may preclude optimal assessment. To detect an endoleak, one study with 52 patients found an increased sensivity of 92.9% using magnetic resonance compared with 44% sensivity with biphasic CT, calling into question the superiority of CT (Pitton et al. 2005). Moreover, a meta-analysis showed MRA to be potentially more sensitive than CTA for the detection of endoleaks, particularly for type II endoleaks (Habets et al. 2013). Four-dimensional phase contrast MRA has the capacity to visualize flow dynamics within the aorta, and increased sensivity for the detection of endoleaks relative to CTA (Katahashi et al. 2019; Sakata et al. 2016).
Otherwise, DUS does not require nephrotoxic contrast or radiation. Several studies on color duplex ultrasound (CDUS) and contrast-enhanced ultrasound (CEUS) have had conflicting opinions regarding their diagnostic value relative to CTA. In a meta-analysis, CDUS sensivity to detect type I and III endoleaks was 0.83 and specificity was 1 (Karthikesalingam et al. 2012). The use of ultrasound contrast agent may allow identifying endoleaks that are not detected with CT (Napoli et al. 2004). Thus, some authors think that CEUS may replace CT in surveillance programs after EVAR (Bredahl et al. 2016). A meta-analysis of 42 studies found CEUS to be superior to CDUS for ruling in endoleaks (Abraha et al. 2017). Similarly, in another meta-analysis of 18 studies the authors found that CEUS had higher sensivity and comparable specificity to CTA for the detection of endoleaks (Harky et al. 2019). According to this, a systematic review found that CEUS and MRA are more accurate than CT for the detection of endoleaks, but they are not better than CT for detecting types I and III endoleaks specifically (Guo et al. 2016).
Regarding capability of angiography to detect endoleaks, a comparative analysis showed a sensivity of 63% whereas sensivity with CT was 96% (Armerding et al. 2000). More recent studies found a sensivity between 69% (Ashoke et al. 2005) and 86% (Manning et al. 2009). In the setting of an endoleak identified on the previously cited imaging methods, angiography is an essential modality for further diagnostic characterization and treatment.
Interestingly, and regarding the limitations of angiography, Blackwood et al. created an in vitro model in an experimental study. Measurements of pressure and angiography images were recorded in three scenarios: no endoleak, type I endoleak with inflow and sac outflow and a type I endoleak with inflow but no sac outflow. In the second scenario, aneurysm sac pressure was lower than the systemic and the endoleak was visible at 30 s. In the last scenario sac pressure was higher than the systemic so that net flow was zero and visibility of an endoleak was confirmed after 9 min. Consequently, they concluded that the endoleak could only be visualized with markedly delayed imaging and not with standard angiography like that used in clinical practice (Blackwood et al. 2016). Therefore, endotension may represent an undiagnosed endoleak, particularly type I.
Fabric porosity
The possible influence of fabric porosity in the pressure transmission to the aneurysm sac is another controversial point. Initially it was proposed as one of the possible causes of endotension although afterwards it was considered as type IV endoleak.
Available endografts are made of different materials and each one has its corresponding porosity grade. Initially, some clinical data suggested that PTFE stent-grafts could not prevent the sac enlargement despite of the aneurysm exclusion in the absence of endoleak. Moreover, some studies observed a lower incidence in the regression of the aneurysm sac in patients that underwent treatment with the original Excluder stent-graft in comparison with other devices (Cho et al. 2004; Bertges et al. 2003; Rhee et al. 2000; Trocciola et al. 2006). Because of the publication of these findings, the Excluder endograft was modified in 2004, incorporating an additional low-permeability layer to reduce porosity.
In an experimental study in a canine model, Trocciola et al. found that stent-graft treatment reduces intra-aneurysmal pressure to < 30% of systemic pressure (nonpulsatile). However, significantly greater pressure was observed after exclusion with PTFE stent-grafts compared with Dacron grafts (Trocciola et al. 2006). Histology showed that those aneurysms that were excluded with the original Excluder stent-graft (thin-wall ePTFE) contained poorly organized thrombus and fibrin deposition, which could be indicative of active remodeling and continued influx of transudated serum. In contrast, aneurysms excluded by Dacron stent-grafts resulted in thrombi that were well organized and chronically composed mostly of granulation tissue. Dense mature collagenous connective tissue was also found in this group.
Haider et al. compared the sac behavior after aneurysm treatment with the original Excluder device, with the low-permeability Excluder device or with the Zenith stent-graft. At 1 year, sac regression rate was 25%, 63.9% and 65.3%, respectively. Consequently, they concluded that low-porosity fabric seems to be an important factor in early aneurysm sac shrinkage (Haider et al. 2006). Reinforcing this conclusion, the long-term results with this new Excluder device confirmed sac regression in 63% at 5 years. Interestingly, sac enlargement was observed only in the setting of a current or previous endoleak, with no cases of hygroma formation noted (Hogg et al. 2011).
A previously cited experimental study compared the new Excluder stent-graft to other available devices (Zenith and AneuRx) and demonstrated that there were no significant differences in the transmitted pressure to the sac among the analyzed devices. In addition, the pulse pressure was identical for all of them (Bosman et al. 2009).
In another study, also in a canine model, Hynecek et al. made a comparison among three distinct stent-grafts: the Trivascular Enovus (nonporous PTFE), the original Excluder (porous PTFE) and the Medtronic AneuRx (Dacron) (Hynecek et al. 2007). Within 24 h after exclusion pulse pressure within the sac tapered to less than 20% of systemic pressure for all three stent graft types. However, throughout the postoperative period significantly lower intra-aneurysmal pressures were present in those aneurysms that were not treated with the porous PTFE device. Histologic analysis of the Excluder-treated aneurysms demonstrated poorly organized fibrin deposition suggestive of acute thrombus. Dacron-treated aneurysms demonstrated mature well-organized collagenous connective tissue. Those aneurysms treated with nonporous PTFE showed characteristics of acute and chronic thrombus. Authors did not find hygromas, although the study period did not exceed 30 days.
Regarding the fabric porosity, it should be underscored that although cases of sac enlargement without a detected endoleak were documented in patients treated with the original Excluder device, the endotension-related rupture incidence was very low. In fact, Kong et al. reviewed data from the multicenter phase I and II clinical trials and reported no endotension-related aneurysm rupture (Kong et al. 2005).
Fluid accumulation
Regarding the fluid accumulation theory, some cases of hygroma have been reported, describing a gelatinous material within the aneurysm sac (Williams 1998; Risberg et al. 2001; Thoo et al. 2004). One study included four patients with aneurysm sac expansion: one patient had undergone open surgery using a PTFE graft, and three cases had undergone treatment with endografts (two PTFE endografts and one Dacron endograft). The aspirated fluid was described as highly viscous and the analysis reported local hyperfibrinolysis in the sac with signs of local coagulation activation. The authors, Risberg et al., proposed the hygroma theory as a pathophysiological mechanism for endotension (Risberg et al. 2001).
Another study included five cases of symptomatic patients with late sac enlargement, all of them had undergone open repair of abdominal aortic aneurysm using PTFE grafts. Four of them underwent laparotomy and a seroma containing firm rubbery gelatinous material was found in all cases (Thoo et al. 2004). This fact led the authors to suppose that the most likely cause of sac enlargement was the fluid flow from aortic lumen to the aneurysm sac through the graft. It is important to consider that the incidence of symptomatic aneurysm enlargement in the patients after open repair with PTFE grafts was low (2.3%). It also has to be highlighted that the PTFE grafts were thin-walled and differed in porosity compared with PTFE used in the manufacture of Excluder endografts.
Intermittent endoleaks
Seven cases described as intermittent endoleaks and four cases described as posture-dependent endoleaks were reported in an article (May and Harris 2012). The first case was a patient with aneurysm sac enlargement and no demonstrated endoleak. When the patient underwent reintervention by open surgery, they found a jet of blood when the endograft was subjected to positional changes. They also reported two cases in which the endoleak could only be imaged, using duplex, by changing the patient’s position on the examination table. May et al. concluded that patients with this condition could be considered to have endotension and that the ultrasound would be the most suitable diagnosis test in these cases.
Discussion
Evidence indicates that aneurysmal sac pressure decreases after endovascular repair. It is widely assumed that this is why most of aneurysms shrink or remain unchanged in size. When there is a persistent endoleak, the intrasac pressure remains high, consequently aneurysms often grow. In some cases, aneurysm sac grows without detecting an associated endoleak. Several hypotheses were proposed to explain these cases. After the review of the literature, some theories have been reinforced whereas others have been weakened.
Evidence derived from experimental studies indicates that pressure is transmitted through thrombus in the case of short and wide occluded channels. Thus, pressure could be transmitted to the excluded aneurysm sac if there is a wide area of thrombus lining the attachment sites of the endograft and the distance to the sac is short. Similarly, the pressure could be also transmitted through thrombus originated over the orifices of aortic or iliac branches of the aneurysm.
Another point to highlight is the limitation of current imaging techniques to detect some endoleaks, particularly if the flow is low. A foolproof imaging technique for endoleak diagnosis is still not available. CT remains the preferred method for diagnosis, but a meta-analysis showed MRA to be potentially more sensitive than CTA for the detection of endoleaks, particularly for type II endoleaks. Furthermore, the results from two meta-analysis and a systematic review concluded that CEUS and MRA can be superior to CT for the detection of some endoleaks. In addition, new technologies such as PCD CT and four-dimensional phase contrast MRA, have potential for better visualization and increased sensivity for the detection of endoleaks relative to CTA. Thus, these new technologies could allow decreasing the number of cases in which the endoleak is not identified. On the other hand, it is also interesting to underscore the limitations of angiography to identify a type I endoleak with no sac outflow. The experimental study of Blackwood et al. demonstrated that this type of endoleak could only be visualized with markedly delayed imaging and not with standard angiography.
In contrast, other etiological theories currently seem less plausible. The experimental study of Bosman et al. determined that the pressure transmission through the commercially available stent-grafts wall is clinically irrelevant and the influence of graft rigidity on endotension is unlikely.
Regarding the fabric porosity theory, it seems unlikely that porosity of the currently available devices is the cause of aneurysmal enlargement. Furthermore, in that case, demonstration with imaging methods would be unlikely as well. However, an endoleak originated by stent-graft fabric rupture could be more likely identified, but they are rare. Similarly, it could be considered that reported cases of fluid accumulation were related to fabric porosity of the PTFE grafts or endografts.
Special mention should be made of the intermittent endoleaks. They were described as depending on postural changes and consequently, there is a limitation of imaging methods for its detection. Given the number of reported cases, it could be considered that they are unusual and sporadic.
Summarizing, experimental studies call into question that “causes other than pressure” apply stress to the aneurysm wall conditioning its enlargement. For this reason, “endopressure” would be a better fit to the concept that it is aimed to be defined, but this term would also include those cases with a detected endoleak. On the other hand, sac expansion can be objectified, but sac pressurization is not objectified throughout conventional follow-up after EVAR. This is why the use of another term such as “Sac Expansion Without Evident Leak” (SEWEL) would be more precise than endotension.
Conclusions
Evidence suggests that the most likely mechanisms of persistent intra-sac high pressure are two: the endoleak occur but it is not identified (probably a type I or low-flow type II) or pressure is transmitted through thrombus in the case of short and wide occluded channels between the arterial lumen and the excluded aneurysm sac (at the attachment sites of the endograft or through side branches orifices).
On the other hand, type IV endoleak related to fabric porosity would be unlikely with current devices. In the event of this issue, detection by means of the available imaging methods would be unlikely as well.
In our opinion, the used terminology is rather confusing. Given the evidence of existing studies, it would need to be updated. Any of the cited mechanisms in the preceding paragraph may be the origin of a SEWEL (Sac Expansion Without Evident Leak). A detailed analysis of each individual case will allow guidance of the investigation towards any of them.
Availability of data and materials
Not applicable.
Abbreviations
- CT:
-
Computed tomography
- PTFE:
-
Polytetrafluoroethylene
- DUS:
-
Duplex ultrasound
- MRA:
-
Magnetic resonance angiography
References
Abraha I, Luchetta ML, De Florio R, Cozzolino F, Casazza G, Duca P et al (2017) Ultrasonography for endoleak detection after endoluminal abdominal aortic aneurysm repair. Cochrane Database Syst Rev 6:CD010296
Armerding MD, Rubin GD, Beaulieu CF, Slonim SM, Olcott EW, Samuels SL, Jorgensen MJ, Semba CP, Jeffrey RB Jr, Dake MD (2000) Aortic aneurysmal disease: assessment of stent-graft treatment-CT versus conventional angiography. Radiology. 215(1):138–146. https://doi.org/10.1148/radiology.215.1.r00ap28138
Ashoke R, Brown LC, Rodway A, Choke E, Thompson MM, Greenhalgh RM, Powell JT (2005) Color duplex ultrasonography is insensitive for the detection of endoleak after aortic endografting: a systematic review. J Endovasc Ther 12(3):297–305. https://doi.org/10.1583/04-1479R.1
Bertges DJ, Chow K, Wyers MC, Landsittel D, Frydrych AV, Stavropoulos W, Tan WA, Rhee RY, Fillinger MF, Fairman RM, Makaroun MS (2003) Abdominal aortic aneurysm size regression after endovascular repair is endograft dependent. J Vasc Surg 37(4):716–723. https://doi.org/10.1067/mva.2003.212
Blackwood S, Mix D, Chandra A, Dietzek AM (2016) A model to demonstrate that endotension is a nonvisualized type I endoleak. J Vasc Surg 64(3):779–787. https://doi.org/10.1016/j.jvs.2015.04.422
Bosman WM, Hinnen JW, Rixen DJ, Hamming JF (2009) Effect of stent-graft compliance on endotension after EVAR. J Endovasc Ther 16(1):105–113. https://doi.org/10.1583/08-2505.1
Bredahl KK, Taudorf M, Lönn L, Vogt KC, Sillesen H, Eiberg JP (2016) Contrast Enhanced Ultrasound can Replace Computed Tomography Angiography for Surveillance After Endovascular Aortic Aneurysm Repair. Eur J Vasc Endovasc Surg 52(6):729–734. https://doi.org/10.1016/j.ejvs.2016.07.007
Cho JS, Dillavou ED, Rhee RY, Makaroun MS (2004) Late abdominal aortic aneurysm enlargement after endovascular repair with the excluder device. J Vasc Surg 39(6):1236–1241; discussion 2141-2. https://doi.org/10.1016/j.jvs.2004.02.038
Chuter T, Ivancev K, Malina M, Resch T, Brunkwall J, Lindblad B, Risberg B (1997) Aneurysm pressure following endovascular exclusion. Eur J Vasc Endovasc Surg 13(1):85–87. https://doi.org/10.1016/S1078-5884(97)80056-1
Dangelmaier J, Bar-Ness D, Daerr H, Muenzel D, Si-Mohamed S, Ehn S, Fingerle AA, Kimm MA, Kopp FK, Boussel L, Roessl E, Pfeiffer F, Rummeny EJ, Proksa R, Douek P, Noël PB (2018) Experimental feasibility of spectral photon-counting computed tomography with two contrast agents for the detection of endoleaks following endovascular aortic repair. Eur Radiol 28(08):3318–3325. https://doi.org/10.1007/s00330-017-5252-7
Gawenda M, Jaschke G, Winter S, Wassmer G, Brunkwall J (2003) Endotension as a result of pressure transmission through the graft following endovascular aneurysm repair--an in vitro study. Eur J Vasc Endovasc Surg 26(5):501–505. https://doi.org/10.1016/S1078-5884(03)00378-2
Gawenda M, Knez P, Winter S, Jaschke G, Wassmer G, Schmitz-Rixen T, Brunkwall J (2004) Endotension is influenced by wall compliance in a latex aneurysm model. Eur J Vasc Endovasc Surg 27(1):45–50. https://doi.org/10.1016/j.ejvs.2003.10.013
Gilling-Smith G, Brennan J, Harris P, Bakran A, Gould D, McWilliams R (1999) Endotension after endovascular aneurysm repair: definition, classification, and strategies for surveillance and intervention. J Endovasc Surg 6(4):305–307. https://doi.org/10.1583/1074-6218(1999)006<0305:EAEARD>2.0.CO;2
Guo Q, Zhao J, Huang B, Yuan D, Yang Y, Zeng G, Xiong F, du X (2016) A Systematic Review of Ultrasound or Magnetic Resonance Imaging Compared With Computed Tomography for Endoleak Detection and Aneurysm Diameter Measurement After Endovascular Aneurysm Repair. J Endovasc Ther 23(6):936–943. https://doi.org/10.1177/1526602816664878
Habets J, Zandvoort HJ, Reitsma JB, Bartels LW, Moll FL, Leiner T et al (2013) Magnetic resonance imaging is more sensitive than computed tomography angiography for the detection of endoleaks after endovascular abdominal aortic aneurysm repair: a systematic review. Eur J Vasc Endovasc Surg 45(04):340–350. https://doi.org/10.1016/j.ejvs.2012.12.014
Haider SE, Najjar SF, Cho JS, Rhee RY, Eskandari MK, Matsumura JS et al (2006) Sac behavior after aneurysm treatment with the Gore excluder low-permeability aortic endoprosthesis: 12-month comparison to the original excluder device. J Vasc Surg 44(4):694–700. https://doi.org/10.1016/j.jvs.2006.06.018
Harky A, Zywicka E, Santoro G, Jullian L, Joshi M, Dimitri S (2019) Is contrast-enhanced ultrasound (CEUS) superior to computed tomography angiography (CTA) in detection of endoleaks in post-EVAR patients? A systematic review and meta-analysis. J Ultrasound 22(01):65–75. https://doi.org/10.1007/s40477-019-00364-7
Hogg ME, Morasch MD, Park T, Flannery WD, Makaroun MS, Cho JS (2011) Long-term sac behavior after endovascular abdominal aortic aneurysm repair with the excluder low-permeability endoprosthesis. J Vasc Surg 53(5):1178–1183. https://doi.org/10.1016/j.jvs.2010.11.045
Hynecek RL, Sadek M, Derubertis BG, Ryer EJ, Choi J, Hsu S et al (2007) Evaluation of pressure transmission and intra-aneurysmal contents after endovascular repair using the Trivascular Enovus expanded polytetrafluoroethylene stent graft in a canine model of abdominal aortic aneurysm. J Vasc Surg 46(5):1005–1013. https://doi.org/10.1016/j.jvs.2007.06.041
Iezzi R, Cotroneo AR, Filippone A, Di Fabio F, Quinto F, Colosimo C et al (2006) Multidetector CT in abdominal aortic aneurysm treated with endovascular repair: are unenhanced and delayed phase enhanced images effective for endoleak detection? Radiology. 241(3):915–921. https://doi.org/10.1148/radiol.2413050959
Iezzi R, Cotroneo AR, Filippone A, Santoro M, Basilico R, Storto ML (2008) Multidetector-row computed tomography angiography in abdominal aortic aneurysm treated with endovascular repair: evaluation of optimal timing of delayed phase imaging for the detection of low-flow endoleaks. J Comput Assist Tomogr 32(4):609–615. https://doi.org/10.1097/RCT.0b013e31814b271d
Javor D, Wressnegger A, Unterhumer S, Kollndorfer K, Nolz R, Beitzke D, Loewe C (2017) Endoleak detection using single-acquisition split-bolus dual-energy computer tomography (DECT). Eur Radiol 27(04):1622–1630. https://doi.org/10.1007/s00330-016-4480-6
Karthikesalingam A, Al-Jundi W, Jackson D, Boyle JR, Beard JD, Holt PJ et al (2012) Systematic review and meta-analysis of duplex ultrasonography, contrast-enhanced ultrasonography or computed tomography for surveillance after endovascular aneurysm repair. Br J Surg 99(11):1514–1523. https://doi.org/10.1002/bjs.8873
Katahashi K, Sano M, Takehara Y, Inuzuka K, Sugiyama M, Alley MT et al (2019) Flow dynamics of type II endoleaks can determine sac expansion after endovascular aneurysm repair using four-dimensional flow-sensitive magnetic resonance imaging analysis. J Vasc Surg 70(01):107–116.e1
Kong LS, MacMillan D, Kasirajan K, Milner R, Dodson TF, Salam AA, Smith RB III, Chaikof EL (2005) Secondary conversion of the Gore excluder to operative abdominal aortic aneurysm repair. J Vasc Surg 42(4):631–638. https://doi.org/10.1016/j.jvs.2005.05.056
Kougias P, Bismuth J, Huynh TT, Lin PH (2008) Symptomatic aneurysm rupture without bleeding secondary to endotension 4 years after endovascular repair of an abdominal aortic aneurysm. J Endovasc Ther 15(6):702–705. https://doi.org/10.1583/08-2391.1
Lin PH, Bush RL, Katzman JB, Zemel G, Puente OA, Katzen BT, Lumsden AB (2003) Delayed aortic aneurysm enlargement due to endotension after endovascular abdominal aortic aneurysm repair. J Vasc Surg 38(4):840–842. https://doi.org/10.1016/S0741-5214(03)00468-3
Manning BJ, O'Neill SM, Haider SN, Colgan MP, Madhavan P, Moore DJ (2009) Duplex ultrasound in aneurysm surveillance following endovascular aneurysm repair: a comparison with computed tomography aortography. J Vasc Surg 49(1):60–65. https://doi.org/10.1016/j.jvs.2008.07.079
Marty B, Sanchez LA, Ohki T, Wain RA, Faries PL, Cynamon J, Marin ML, Veith FJ (1998) Endoleak after endovascular graft repair of experimental aortic aneurysms: does coil embolization with angiographic "seal" lower intraaneurysmal pressure? J Vasc Surg 27(3):454–461. https://doi.org/10.1016/S0741-5214(98)70320-9
May J, Harris JP (2012) Intermittent, posture-dependent, and late endoleaks after endovascular aortic aneurysm repair. Semin Vasc Surg 25(3):167–173. https://doi.org/10.1053/j.semvascsurg.2012.07.004
Mehta M, Ohki T, Veith FJ, Lipsitz EC (2001) All sealed endoleaks are not the same: a treatment strategy based on an ex-vivo analysis. Eur J Vasc Endovasc Surg 21(6):541–544. https://doi.org/10.1053/ejvs.2001.1349
Meier GH, Parker FM, Godziachvili V, Demasi RJ, Parent FN (2001) Gayle RG Endotension after endovascular aneurysm repair: the Ancure experience. J Vasc Surg 34(3):421–426. https://doi.org/10.1067/mva.2001.117145
Napoli V, Bargellini I, Sardella SG, Petruzzi P, Cioni R, Vignali C, Ferrari M, Bartolozzi C (2004) Abdominal aortic aneurysm: contrast-enhanced US for missed endoleaks after endoluminal repair. Radiology. 233(1):217–225. https://doi.org/10.1148/radiol.2331031767
Parodi JC, Berguer R, Ferreira LM, La Mura R, Schermerhorn ML (2001) Intra-aneurysmal pressure after incomplete endovascular exclusion. J Vasc Surg 34(5):909–914. https://doi.org/10.1067/mva.2001.119038
Pitton MB, Schweitzer H, Herber S, Schmiedt W, Neufang A, Kalden P, Thelen M, Düber C (2005) MRI versus helical CT for endoleak detection after endovascular aneurysm repair. AJR Am J Roentgenol 185(5):1275–1281. https://doi.org/10.2214/AJR.04.0729
Rhee RY, Eskandari MK, Zajko AB, Makaroun MS (2000) Long-term fate of the aneurysmal sac after endoluminal exclusion of abdominal aortic aneurysms. J Vasc Surg 32(4):689–696. https://doi.org/10.1067/mva.2000.110172
Risberg B, Delle M, Eriksson E, Klingenstierna H, Lönn L (2001) Aneurysm sac hygroma: a cause of endotension. J Endovasc Ther 8(5):447–453. https://doi.org/10.1177/152660280100800504
Rozenblit AM, Patlas M, Rosenbaum AT, Okhi T, Veith FJ, Laks MP, Ricci ZJ (2003) Detection of endoleaks after endovascular repair of abdominal aortic aneurysm: value of unenhanced and delayed helical CT acquisitions. Radiology. 227(2):426–433. https://doi.org/10.1148/radiol.2272020555
Sakata M, Takehara Y, Katahashi K, Sano M, Inuzuka K, Yamamoto N, Sugiyama M, Sakahara H, Wakayama T, Alley MT, Konno H, Unno N (2016) Hemodynamic analysis of endoleaks after endovascular abdominal aortic aneurysm repair by using 4-dimensional flow-sensitive magnetic resonance imaging. Circ J 80(08):1715–1725. https://doi.org/10.1253/circj.CJ-16-0297
Sanchez LA, Faries PL, Marin ML, Ohki T, Parsons RE, Marty B, Soeiro D, Olivieri S, Veith FJ (1997) Chronic intraaneurysmal pressure measurement: an experimental method for evaluating the effectiveness of endovascular aortic aneurysm exclusion. J Vasc Surg 26(2):222–230. https://doi.org/10.1016/S0741-5214(97)70182-4
Thoo CH, Bourke BM, May J (2004) Symptomatic sac enlargement and rupture due to seroma after open abdominal aortic aneurysm repair with polytetrafluoroethylene graft: implications for endovascular repair and endotension. J Vasc Surg 40(6):1089–1094. https://doi.org/10.1016/j.jvs.2004.08.057
Trocciola SM, Dayal R, Chaer RA, Lin SC, DeRubertis B, Ryer EJ, Hynececk RL, Pierce MJ, Prince M, Badimon J, Marin ML, Fuster V, Kent KC, Faries PL (2006) The development of endotension is associated with increased transmission of pressure and serous components in porous expanded polytetrafluoroethylene stent-grafts: characterization using a canine model. J Vasc Surg 43(1):109–116. https://doi.org/10.1016/j.jvs.2005.09.023
White GH, May J (2000) How should endotension be defined? History of a concept and evolution of a new term. J Endovasc Ther 7(6):435–438. https://doi.org/10.1177/152660280000700601
White GH, May J, Petrasek P, Waugh R, Stephen M, Harris J (1999) Endotension: an explanation for continued AAA growth after successful endoluminal repair. J Endovasc Surg 6(4):308–315. https://doi.org/10.1583/1074-6218(1999)006<0308:EAEFCA>2.0.CO;2
Williams GM (1998) The management of massive ultrafiltration distending the aneurysm sac after abdominal aortic aneurysm repair with a polytetrafluoroethylene aortobiiliac graft. J Vasc Surg 28(3):551–555. https://doi.org/10.1016/S0741-5214(98)70144-2
Yoshitake A, Hachiya T, Itoh T, Kitahara H, Kasai M, Kawaguchi S et al (2015) Nonvisualized type III endoleak masquerading as endotension: a case report. Ann Vasc Surg 29(3):595.e15–595.e17
Acknowledgements
Not applicable.
Funding
This study was not supported by any funding.
Author information
Authors and Affiliations
Contributions
ATB: conception, design, acquisition, analysis, interpretation, drafted. MMH: revision. The authors read and approved the final manuscript.
Corresponding author
Ethics declarations
Ethics approval and consent to participate
Not applicable.
Consent for publication
Not applicable.
Competing interests
The authors declare that they have no competing interests.
Additional information
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Rights and permissions
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
About this article
Cite this article
Torres-Blanco, Á., Miralles-Hernández, M. Endotension: twenty years of a controversial term. CVIR Endovasc 4, 46 (2021). https://doi.org/10.1186/s42155-021-00238-2
Received:
Accepted:
Published:
DOI: https://doi.org/10.1186/s42155-021-00238-2
Keywords
- Endotension
- Abdominal aortic aneurysm
- Aorta
- Endovascular aneurysm repair
- Endoleak