Skin necrosis is a consequence of local devascu-larisation, induced by multiple causal factors like infection, macroangiopathy or microangi-opathy, hyperpressure coming from outside or inside, or high-velocity trauma (Figs. 1.1, 1.2, 1.3, 1.4, 1.5, and 1.6). Necrosis is a consequence of cascades of events starting on the venous side and then blocking the arterioles and larger arteries.Most of the time, the clinical context is clear enough to determine the origin of the necrosis and the potential risks of extension to the depth or over the surface. In this part, the authors resume the present knowledge on how necrotic tissue develops, which capacity of reperfusion can be expected, how to explore the extent of the necrotic process, and predominantly the vascular investigations mandatory prior to determining a debridement strategy. The capacity to properly treat ischaemic limbs as emergencies, revascular-ise segments of limbs (lower limbs predomi-nantly), and prevent amputation is a real progress, allowed by early diagnosis and accurate strate-gies of revascularisation, using innovative per-forming stents and distal bypasses. In the same time, necrotic and devascularised tissues repre-sent a potential risk for the vascular surgery itself, imposing a local debridement contemporary to the revascularisation procedure.Keeping in mind that a freshly revascularised limb will take some days to eliminate oedema and inflammation stuck into the tissues, the risk of renecrosis remains during this period of time. Amputation itself may be the cause of hyperpres-sure of the suture edges, and the problem of leav-ing a transmetatarsal amputation open is posed, especially due to the emerging capacities of negative-pressure wound therapy (NPWT) to help local angiogenesis and improve the local granulation tissue. Imaging investigations are needed to define the limits of vascular and tissu-lar damages, beyond which debridement is not any more possible or at risk of renecrosis issuing to an amputation.