An expert multidisciplinary panel in the treatment of type B aortic dissection reviewed available literature to develop treatment algorithms using a consensus method. Data from 63 studies published from 2006 to 2012 were retrieved for a total of 1,548 patients treated medically, 1,706 patients who underwent open surgery, and 3,457 patients who underwent thoracic endovascular repair (TEVAR). For acute (first 2 weeks) type B aortic dissection, the pooled early mortality rate was 6.4% with medical treatment and increased to 10.2% with TEVAR and 17.5% with open surgery, mostly for complicated cases. Limited data for treatment of subacute (2 to 6 weeks after onset) type B aortic dissection showed an early mortality rate of 2.8% with TEVAR. In chronic (after 6 weeks) type B aortic dissection, 5-year survival of 60% to 80% was expected with medical therapy because complications were likely. If interventional treatment was applied, the pooled early mortality rate was 6.6% with TEVAR and 8.0% with open surgery. Medical treatment of uncomplicated acute, subacute, and chronic type B aortic dissection is managed with close image monitoring. Hemodynamic instability, organ malperfusion, increasing periaortic hematoma, and hemorrhagic pleural effusion on imaging identify patients with complicated acute type B aortic dissection requiring urgent aortic repair. Recurrence of symptoms, aortic aneurysmal dilation (>55 mm), or a yearly increase of >4 mm after the acute phase are predictors of adverse outcome and need for delayed aortic repair ("complicated chronic aortic dissections"). The expert panel is aware that this consensus document provides proposal for strategies based on nonrobust evidence for management of type B aortic dissection, and that literature results were largely heterogeneous and should be interpreted cautiously.

Ulcerated diabetic foot is a complex problem. Ischaemia, neuropathy and infection are the three pathological components that lead to diabetic foot complications, and they frequently occur together as an aetiologic triad. Neuropathy and ischaemia are the initiating factors, most often together as neuroischaemia, whereas infection is mostly a consequence. The role of peripheral arterial disease in diabetic foot has long been underestimated as typical ischaemic symptoms are less frequent in diabetics with ischaemia than in non-diabetics. Furthermore, the healing of a neuroischaemic ulcer is hampered by microvascular dysfunction. Therefore, the threshold for revascularising neuroischaemic ulcers should be lower than that for purely ischaemic ulcers. Previous guidelines have largely ignored these specific demands related to ulcerated neuroischaemic diabetic feet. Any diabetic foot ulcer should always be considered to have vascular impairment unless otherwise proven. Early referral, non-invasive vascular testing, imaging and intervention are crucial to improve diabetic foot ulcer healing and to prevent amputation. Timing is essential, as the window of opportunity to heal the ulcer and save the leg is easily missed. This chapter underlines the paucity of data on the best way to diagnose and treat these diabetic patients. Most of the studies dealing with neuroischaemic diabetic feet are not comparable in terms of patient populations, interventions or outcome. Therefore, there is an urgent need for a paradigm shift in diabetic foot care; that is, a new approach and classification of diabetics with vascular impairment in regard to clinical practice and research. A multidisciplinary approach needs to implemented systematically with a vascular surgeon as an integrated member. New strategies must be developed and implemented for diabetic foot patients with vascular impairment, to improve healing, to speed up healing rate and to avoid amputation, irrespective of the intervention technology chosen. Focused studies on the value of predictive tests, new treatment modalities as well as selective and targeted strategies are needed. As specific data on ulcerated neuroischaemic diabetic feet are scarce, recommendations are often of low grade.

AND is a frequent sequela of endoluminal repair in the mid-term. Severe AND developed in a small percentage of our patients, compromising integrity of AAA repair. Patients with large aneurysms and aortic necks and patients with aortic neck circumferential thrombus are at high risk for aortic neck enlargement after endoluminal repair of AAA.

Endovascular treatment of iliac aneurysm with hypogastric revascularization through side branched endografts is feasible and safe in the mid-term. When compared with hypogastric embolization, this option leads to similar technical success and reintervention rates. Endoleak and buttock claudication occur frequently in patients with iliac aneurysm treated with hypogastric exclusion, while are uncommon in those with hypogastric revascularization. Side branch endografting for iliac aneurysm may be considered a primary choice in younger, active patients with suitable anatomy, but larger studies and longer postoperative observation periods are needed.

Epidemiologic evidence suggests that patients with diabetes may have a lower incidence of abdominal aortic aneurysm (AAA); however, the link between diabetes and AAA development and expansion is unclear. The aim of this review is to analyze updated evidence to better understand the impact of diabetes on prevalence, incidence, clinical outcome, and expansion rate of AAA. A systematic review of literature published in the last 20 years using the PubMed and Cochrane databases was undertaken. Studies reporting appropriate data were identified and a meta-analysis performed using the generic inverse variance method. Sixty-four studies were identified. Methodological quality was "fair" in 16 and "good" in 44 studies according to a formal assessment checklist (Newcastle-Ottawa). In 17 large population prevalence studies there was a significant inverse association between diabetes and AAA: pooled odds ratio (OR) 0.80; 95% confidence intervals (CI) 0.70-0.90 (p = .0009). An inverse association was also confirmed by pooled analysis of data from smaller prevalence studies on selected populations (OR 0.59; 95% CI 0.35-0.99; p = .05), while no significant results were provided by case-control studies. A significant lower pooled incidence of new AAA in diabetics was found over six prospective studies: OR 0.54; 95% CI 0.31-0.91; p = .03. Diabetic patients showed increased operative (30-day/in-hospital) mortality after AAA repair: pooled OR 1.26; 95% CI 1.10-1.44; p = .0008. The increased operative risk was more evident in studies with 30-day assessment. In the long-term, diabetics showed lower survival rates at 2-5 years, while there was general evidence of lower growth rates of small AAA in patients with diabetes compared to non-diabetics. There is currently evidence to support an inverse relationship between diabetes and AAA development and enlargement, even though fair methodological quality or unclear risk of bias in many available studies decreases the strength of the finding. At the same time, operative and long-term survival is lower in diabetic patients, suggesting increased cardiovascular burden. The higher mortality in diabetics raises the question as to whether AAA repair should be individualized in selected diabetic populations at higher AAA rupture risk.