TY - JOUR
T1 - Type II Endoleak after Endovascular Aneurysm Repair
T2 - Natural History and Treatment Outcomes
AU - Kumar, Liana
AU - Cowled, Prue
AU - Boult, Margaret
AU - Howell, Stuart
AU - Fitridge, Robert
PY - 2017/10
Y1 - 2017/10
N2 - Background The natural history of type II endoleaks and linkage to aneurysm rupture is unclear. Likewise, treatment recommendations are controversial. The aim of this study was to examine the incidence, factors associated with type II endoleaks, and outcomes in an Australia cohort of patients who have undergone endovascular aneurysm repair (EVAR). Methods Data from 693 patients who underwent EVAR between 2009 and 2013 at multiple institutions across Australia were studied. Patients who developed (1) type II endoleak and (2) type II endoleak with sac expansion were compared for preoperative demographics, mortality, sac expansion, aneurysm rupture, and intervention rates. Results A total of 225 patients developed type II endoleak over a mean follow-up of 1.9 years (±1.0 years), out of which 133 spontaneously resolved, 37 were untreated unresolved, and 16 underwent intervention. Type I and III endoleaks occurred in 50 and 19 patients, respectively. Smoking (P = 0.002) and warfarin (P = 0.044) were protective factors for development of type II endoleak, whereas age (P = 0.034), right iliac artery tortuosity (P = 0.031), and right (P = 0.008) and left external iliac diameters (P = 0.028) were risk factors for endoleak. Three patients suffered aneurysm ruptures in the entire cohort. All ruptures occurred in type II endoleak patients, of which two occurred after reintervention and in the absence of sac expansion (>5 mm). Late type II endoleak occurred in 117 patients, out of which 26 had sac expansion. Of those without late type II endoleak, 25 have sac expansion. There was no statistically significant difference in survival between those with and without type II endoleak. Age (P < 0.0001) and smoking (P = 0.001) were significant independent predictive factors for survival in this patient sample. Treatment outcomes were encouraging with most cases involving endoleak resolution (15 of 16 patients) and no sac expansion after intervention (0 of 8 patients with complete follow-up info on sac size). Conclusions Aneurysm rupture in patients with type II endoleak is uncommon in our series. Type II endoleak with sac expansion does not appear to be associated with aneurysm rupture. In this series, most aneurysm ruptures occurred in the absence of documented sac expansion and after reintervention.
AB - Background The natural history of type II endoleaks and linkage to aneurysm rupture is unclear. Likewise, treatment recommendations are controversial. The aim of this study was to examine the incidence, factors associated with type II endoleaks, and outcomes in an Australia cohort of patients who have undergone endovascular aneurysm repair (EVAR). Methods Data from 693 patients who underwent EVAR between 2009 and 2013 at multiple institutions across Australia were studied. Patients who developed (1) type II endoleak and (2) type II endoleak with sac expansion were compared for preoperative demographics, mortality, sac expansion, aneurysm rupture, and intervention rates. Results A total of 225 patients developed type II endoleak over a mean follow-up of 1.9 years (±1.0 years), out of which 133 spontaneously resolved, 37 were untreated unresolved, and 16 underwent intervention. Type I and III endoleaks occurred in 50 and 19 patients, respectively. Smoking (P = 0.002) and warfarin (P = 0.044) were protective factors for development of type II endoleak, whereas age (P = 0.034), right iliac artery tortuosity (P = 0.031), and right (P = 0.008) and left external iliac diameters (P = 0.028) were risk factors for endoleak. Three patients suffered aneurysm ruptures in the entire cohort. All ruptures occurred in type II endoleak patients, of which two occurred after reintervention and in the absence of sac expansion (>5 mm). Late type II endoleak occurred in 117 patients, out of which 26 had sac expansion. Of those without late type II endoleak, 25 have sac expansion. There was no statistically significant difference in survival between those with and without type II endoleak. Age (P < 0.0001) and smoking (P = 0.001) were significant independent predictive factors for survival in this patient sample. Treatment outcomes were encouraging with most cases involving endoleak resolution (15 of 16 patients) and no sac expansion after intervention (0 of 8 patients with complete follow-up info on sac size). Conclusions Aneurysm rupture in patients with type II endoleak is uncommon in our series. Type II endoleak with sac expansion does not appear to be associated with aneurysm rupture. In this series, most aneurysm ruptures occurred in the absence of documented sac expansion and after reintervention.
UR - http://www.scopus.com/inward/record.url?scp=85021694444&partnerID=8YFLogxK
U2 - 10.1016/j.avsg.2017.04.029
DO - 10.1016/j.avsg.2017.04.029
M3 - Article
C2 - 28483626
AN - SCOPUS:85021694444
SN - 0890-5096
VL - 44
SP - 94
EP - 102
JO - Annals of Vascular Surgery
JF - Annals of Vascular Surgery
ER -