M R Scheltinga1, C M A Bruijninckx. 1. Department of Surgery, Máxima Medical Center Veldhoven, de Run 4600, 5500 MB Veldhoven, The Netherlands. m.scheltinga@mmc.nl
Abstract
OBJECTIVES: Some haemodialysis patients with an arteriovenous fistula (AVF) suffer from chronic hand ischaemia (haemodialysis access-induced distal ischaemia, HAIDI). This overview discusses pathophysiological mechanisms of chronic HAIDI with emphasis on the role of steal and loco-regional hypotension. MATERIALS AND METHODS: The literature obtained from Medline and Google using various terms including steal and hand ischaemia was studied for clues on pathophysiology of hand ischaemia in the presence of an AVF. RESULTS: Constructing an arteriovenous anastomosis as in a haemodialysis access leads to augmented blood flows in arm arteries. Due to increased shear stress, these arteries will remodel while hand perfusion pressures are maintained. However, arteries of some dialysis patients with diabetes mellitus and/or severe arteriosclerosis demonstrate insufficient remodelling leading to a gradual loss of perfusion pressures towards the periphery. A blood pressure drop associated with turbulent flow at the arteriovenous anastomosis intensifies the distal hypotension. By contrast, steal (reversal of blood flow) may reflect an upstream arterial stenosis and patent collaterals but its presence has no pathophysiological significance related to hand ischaemia. CONCLUSION: HAIDI is caused by too low forearm and hand blood pressures. Therapy should focus on attenuating the loss of arterial pressure including optimalisation of inflow arteries and/or ligation of the AVF's venous side branches. Surgery aimed at access flow reduction or distal revascularisation is only indicated if these measures fail.
OBJECTIVES: Some haemodialysis patients with an arteriovenous fistula (AVF) suffer from chronic hand ischaemia (haemodialysis access-induced distal ischaemia, HAIDI). This overview discusses pathophysiological mechanisms of chronic HAIDI with emphasis on the role of steal and loco-regional hypotension. MATERIALS AND METHODS: The literature obtained from Medline and Google using various terms including steal and hand ischaemia was studied for clues on pathophysiology of hand ischaemia in the presence of an AVF. RESULTS: Constructing an arteriovenous anastomosis as in a haemodialysis access leads to augmented blood flows in arm arteries. Due to increased shear stress, these arteries will remodel while hand perfusion pressures are maintained. However, arteries of some dialysis patients with diabetes mellitus and/or severe arteriosclerosis demonstrate insufficient remodelling leading to a gradual loss of perfusion pressures towards the periphery. A blood pressure drop associated with turbulent flow at the arteriovenous anastomosis intensifies the distal hypotension. By contrast, steal (reversal of blood flow) may reflect an upstream arterial stenosis and patent collaterals but its presence has no pathophysiological significance related to hand ischaemia. CONCLUSION: HAIDI is caused by too low forearm and hand blood pressures. Therapy should focus on attenuating the loss of arterial pressure including optimalisation of inflow arteries and/or ligation of the AVF's venous side branches. Surgery aimed at access flow reduction or distal revascularisation is only indicated if these measures fail.