Revisão Acesso aberto Revisado por pares

Steal syndrome strategies to preserve vascular access and extremity

2007; Oxford University Press; Volume: 23; Issue: 1 Linguagem: Inglês

10.1093/ndt/gfm673

ISSN

1460-2385

Autores

V. Mickley,

Tópico(s)

Vascular anomalies and interventions

Resumo

causes a retrograde flow in the artery distal to the AV anastomosis and into the AV access. This ‘physiologic’ steal phenomenon can be observed in 73% of AV fistulae and in 91% of access grafts [2]. Approximately 75% of the blood flow through distal radio-cephalic fistulae is supplied by the proximal radial artery, but 25% comes from a patent ulnar artery via the distal radial artery and palmar arch [12]. In elbow fistulae, the periarticular arterial collaterals have the same impact. When an AV fistula is created using healthy vessels, dilatation of the proximal and distal arteries, as well as dilatation of the collaterals around the anastomosis, compensates for enhanced systolic AV flow and also for diastolic retrograde inflow into the fistula. Any vascular pathology affecting one or several of these adaptive mechanisms can causedistalischaemiabyastealmechanism.Arterialstenosisupstreamoftheanastomosispreventsthenecessaryflow increase in the feeding artery; severe peripheral arterial occlusive disease (PAOD) or vasculitis enhance the resistance of distal arteries and simultaneously impair the function of natural collaterals [13]. Under these conditions, during diastole virtually all blood coming from the collaterals is drained into the access [14]. Instead of a steal syndrome stage I (also named steal phenomenon), the further dreaded stages II to IV develop, with clinical signs of peripheral ischaemia. The likelihood that a steal syndrome develops depends more on the severity of arterial pathology and less on the volume of intra-access blood flow.

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