WHAT THIS PAPER ADDS Acute kidney injury (AKI) has been associated with worse post-operative outcomes. The exact proportion of patients who develop AKI after aortic intervention and relevant risk factors are not well described, because of poor study design and inconsistent reporting. This multicentre prospective cohort study has shown that AKI is common after both open and endovascular aortic procedures; this drop in renal function persists after 30 days. Age, baseline renal function and pre-existing cardiovascular disease are the main risk factors. Future research should explore renoprotective strategies in this population, targeting predominantly the elderly, those with existing renal dysfunction or several cardiovascular comorbidities.Objective: The incidence of acute kidney injury (AKI) after open (OAR) or endovascular (EVAR) aortic repair is unknown. This research assessed the proportion of patients who develop AKI after aortic intervention using validated criteria, and explored AKI risk factors. Methods: This was a multicentre national prospective cohort study. Eleven centres recruited patients undergoing EVAR or OAR (September 2017eDecember 2018). Serum creatinine (SCr) and urine outputs were measured over a minimum of 48 h or throughout the index inpatient stay to define post-operative AKI using the Kidney Disease Improving Global Outcomes (KDIGO) criteria. Renal decline at 30 days was calculated using estimated glomerular filtration rate (eGFR) and the Major Adverse Kidney Events (MAKE) 30 day composite endpoint (consisting of: death, new dialysis, > 25% eGFR decline). Results: 300 patients (mean age: 71 years, standard deviation [SD] 4 years; 9% females) were included, who underwent: infrarenal endovascular aneurysm repair (EVAR) 139 patients, fenestrated EVAR (fEVAR) 30, branched EVAR (bEVAR) seven, infrarenal open aneurysm repair (OAR) 98, juxtarenal OAR 26. Overall, 24% of patients developed stage 1 AKI (defined at 48 h as per KDIGO), 2.7% stage 2 AKI and 1% needed renal replacement therapy before discharge. AKI proportions per intervention were: infrarenal EVAR 18%; fEVAR 27%; bEVAR 71%; infrarenal OAR 41%; juxtarenal OAR 63%. Older age (odds ratio [OR] 1.44 for EVAR, 1.58 for OAR), lower baseline eGFR (OR 0.88 EVAR, 0.74 OAR), and ischaemic heart disease (OR 4.42 EVAR, 5.80 OAR) were the main predictors of AKI for infrarenal EVAR and OAR. Overall, 24% developed the MAKE30 endpoint. All patients who died (0.6%) or developed a major cardiac event (5.6%) at one year had developed AKI. Conclusion: AKI and short term renal decline after aortic intervention are common. Age, renal function, and cardiovascular disease are the main risk factors. Research should now focus on AKI prevention in this high risk group.

The UK screening programme began in 2009, and has now been expanded around the UK. Long-term follow-up of the original cohorts continues to demonstrate significant benefits for abdominal aortic aneurysm (AAA)-related and all-cause mortality , and results from the first 5 years of the formal screening programme have demonstrated similar success. Ultrasound scanning is an effective and safe screening tool for the detection of AAA, although a variety of measurement protocols are employed internationally. Key challenges for the future of the programme relate to declining incidence of screen detected aneurysms.  Recent publications have demonstrated a UK incidence of only 1.34%, compared to 4.9-7.2% of men invited for screening in the original trials. Work into increasing engagement amongst the target group, and expanding screening to siblings and women is underway to address this issue. This review describes the evidence behind the screening programme, its justification in addressing AAA as a significant health problem and discusses some of the potential developments in the future.

During periods of ischemia and hypoxia, intracellular adenosine triphosphate stores are rapidly depleted. Its metabolism results in release of purine nucleosides into the systemic circulation. While the potential of purine nucleosides as a biomarker of ischemia has long been recognized, this has been limited by their complex physiological role and inherent instability leading to problematic sampling and prolonged, complex analysis procedures. Purine release has been demonstrated from cerebral tissue in patients undergoing carotid endarterectomy and patients presenting to hospital with stroke and transient ischemic attack. Rises in purine nucleosides have also been demonstrated in patients with angina and myocardial infarction, during systemic hypoxia, exercise, in patients with peripheral arterial disease and during surgery. This article reviews purine nucleoside production in ischemia, the development of purine analysis technology and details results of the studies investigating purine nucleosides as a biomarker of ischemia with suggestions for areas of future research.

Surgical site infections (SSIs) of groin wounds are a common and potentially preventable cause of morbidity, mortality, and healthcare costs in vascular surgery. Our aim was to define the contemporaneous rate of groin SSIs, determine clinical sequelae, and identify risk factors for SSI. An international multicentre prospective observational cohort study of consecutive patients undergoing groin incision for femoral vessel access in vascular surgery was undertaken over 3 months, follow-up was 90 days. The primary outcome was the incidence of groin wound SSI. 1337 groin incisions (1039 patients) from 37 centres were included. 115 groin incisions (8.6%) developed SSI, of which 62 (4.6%) were superficial. Patients who developed an SSI had a significantly longer length of hospital stay (6 versus 5 days, P = .005), a significantly higher rate of post-operative acute kidney injury (19.6% versus 11.7%, P = .018), with no significant difference in 90-day mortality. Female sex, Body mass index≥30 kg/m 2 , ischaemic heart disease, aqueous betadine skin preparation, bypass/patch use (vein, xenograft, or prosthetic), and increased operative time were independent predictors of SSI. Groin infections, which are clinically apparent to the treating vascular unit, are frequent and their development carries significant clinical sequelae. Risk factors include modifiable and non-modifiable variables.

Objectives: In periods of cerebral ischaemia, adenosine triphosphate is metabolised, leading to accumulation of adenosine inosine and hypoxanthine. These can be measured in real time using peripheral blood samples intraoperatively. The primary aim of this study was to describe changes in purine concentrations in a cohort of patients undergoing carotid endarterectomy under general anaesthetic, and to evaluate correlation between changes in values with major perioperative steps. The secondary aim was to compare changes in concentrations with a previous cohort of patients who had undergone carotid endarterectomy under local anaesthetic. Methods: This was a prospective observational study. Purine concentrations were determined from arterial line samples and measured via an amperometric biosensor at specific time points during carotid endarterectomy. Mean arterial pressure was manipulated to maintain steady cerebral perfusion pressure throughout the procedure. These results were analysed against data from a cohort of patients who underwent carotid endarterectomy under local anaesthetic in previously published work. Results: Valid results were obtained for 37 patients. Purine concentrations at baseline were 3.02 ± 1.11 µM and 3.16 ± 1.85 µM for the unshunted and shunted cohorts, respectively. There was no significant change after 30 min of carotid clamping at 2.07 ± 0.89 and 2.4 ± 3.09 µM, respectively (both p > 0.05). Peak purine during the clamp phase in the loco-regional anaesthetic cohort was 6.70 ± 3.4 µM, which was significantly raised compared to both general anaesthetic cohorts (p = 0.004). There were no perioperative neurological events in either cohort. Conclusion: This small study does not demonstrate conclusive evidence that purine nucleosides can be used as a marker of cerebral ischaemia; the comparisons to the loco-regional anaesthetic data offer information about differences in the cerebral adenosine triphosphate metabolism between general anaesthetic and loco-regional anaesthetic. We hypothesise that the lack of a rise in purine nucleosides under general anaesthetic may be caused by a decrease in the cerebral metabolic rate and loss of metabolic rate-blood flow coupling caused by general anaesthetic agents.