Aortic Rupture during Endovascular Aneurysm Repair. Report of Our Experience and Review of the Literature.

BACKGROUND: Aortic neck wall rupture during endovascular repair of abdominal aortic aneurysms (EVAR) is an underreported potentially fatal complication. Only a few cases have been reported. The main cause of this complication is repeated attempts at balloon inflation or overdilation to treat an intraoperative Type 1a endoleak. We report three cases complicated by procedure-related aortic neck wall rupture during EVAR. We also review the literature regarding the causes and outcomes of this complication. METHODS: Medical records of all patients undergoing EVAR between January 2009 and March 2019 were retrospectively reviewed. RESULTS: Overall, 824 EVAR procedures were performed, and rupture of the aortic neck wall was observed in three patients. In all cases, a Type 1a endoleak was observed and, in all cases, repeated ballooning attempts had been performed to resolve the endoleaks. In all cases, conversion to open repair was performed and all patients survived. CONCLUSION: In cases of Type 1a endoleak, a maximum of two ballooning attempts should be performed even if a Type 1a endoleak persists. In case of intraoperative aortic neck wall rupture, control of the hemorrhage should be achieved immediately by advancing the balloon above the site of rupture. Emergency surgical conversion in case of hemodynamic stability is the first choice. According to the literature, emergency surgical conversion, especially in cases of endograft with suprarenal fixation, is associated with significant morbidity and mortality rates, mainly due to hemorrhage and to the length of the procedure required to repair the aortic neck wall injury.

Population seroprevalence study after a West Nile virus lineage 2 epidemic, Greece, 2010.

INTRODUCTION: During summer 2010, 262 human cases including 35 deaths from West Nile virus (WNV) infection were reported from Central Macedonia, Greece. Evidence from mosquitoes, birds and blood donors demonstrated that the epidemic was caused by WNV lineage 2, which until recently was considered of low virulence. We conducted a household seroprevalence study to estimate the spread of infection in the population during the epidemic, ascertain the relationship of infection to clinical disease, and identify risk factors for infection. METHODS: We used a two-stage cluster design to select a random sample of residents aged ≥18 years in the outbreak epicentre. We collected demographic, medical, and risk factor data using standard questionnaires and environmental checklists, and tested serum samples for presence of WNV IgG and IgM antibodies using ELISA. RESULTS: Overall, 723 individuals participated in the study, and 644 blood samples were available. Weighted seropositivity for IgG antibodies was 5.8% (95% CI: 3.8-8.6; n=41). We estimated that about 1 in 130 (1:141 to 1:124) infected individuals developed WNV neuroinvasive disease, and approximately 18% had clinical manifestations attributable to their infection. Risk factors for infection reflected high exposure to mosquitoes; rural residents were particularly at risk (prevalence ratio: 8.2, 95% CI: 1.1-58.7). DISCUSSION: This study adds to the evidence that WNV lineage 2 strains can cause significant illness, demonstrating ratios of infection to clinical disease similar to those found previously for WNV lineage 1.

Outbreak of West Nile virus infection in Greece, 2010.

During 2010, an outbreak of West Nile virus infection occurred in Greece. A total of 197 patients with neuroinvasive disease were reported, of whom 33 (17%) died. Advanced age and a history of heart disease were independently associated with death, emphasizing the need for prevention of this infection in persons with these risk factors.