GUIDELINES [ back to index ]
21. Management of ischemia (1)
*1 Medical history
• Some patients are at increased risk of developing hand ischaemia after creation of a vascular access, particularly when the brachial artery is the inflow vessel to the fistula. Risk factors are repeated access surgery on the same extremity, older age, small size of the brachial artery, diabetes and peripheral vascular disease 1. Patients are often symptomatic at the moment the access has been created 1 and, therefore, they should be closely monitored during the first 24 hours after access creation.
*2 Clinical staging of ischaemia
• Clinical signs and symptoms of steal syndrome do not differ from those of leg ischaemia. Therefore, it can be classified according to Fontaine’s classification
Stage I, a reduced wrist-brachial pressure index, with coldness of the hand and discolouration (pale or bluish) may be noticed.
Stage II, intermittent pain during haemodialysis 2, exertion or arm elevation occurs.
Stage III, ischaemic rest pain develops.
Stage IV, ulceration and necrosis with or without rest pain develops.
• Symptomatic steal is associated with reduced wrist-to-brachial blood pressure index (< 0.6) as measured by digital photoplethysmography, with blood pressure cuff and Doppler probe, or by transcutaneous pO2 measurement 3. The cuff and Doppler method can be done in the clinic, on the ward or in the operating theatre.
• In the differential diagnosis of rest pain, ischaemic monomelic neuropathy, uraemic or diabetic neuropathy, secondary hyperparathyroidism, carpal tunnel syndrome and venous hypertension with ulcerative skin changes have to be considered 4 5.
*3 Surgical intervention
• Ischaemia can occur at any time, directly after the creation of a vascular access or much later. Irreversible damage can be caused to nerves within hours due to severe ischaemia, labelled ischaemic monomelic neuropathy. Therefore, patients with significantly impaired nerve function, motor or sensory, must be treated as an emergency.
*4 “Wait and see”
• Stage I and II steal syndrome in both A/V fistulas and grafts can be closely observed and treated conservatively (wearing gloves).
*5 Check for deterioration
• Especially in A/V fistulas already at stage I of ischaemia, close clinical monitoring must be performed. Due to the tendency of flow to increase over time, stage I disease may deteriorate. Monitoring consists of regularly asking the patient about symptoms of exertional or rest pain, increasing coldness and colour changes of the hand, examining the hand for development of ischaemic lesions, and assessing the wrist brachial pressure index.
• The onset of vascular steal can be delayed up to several months after surgery 6.
*6 Access graft
• Contrary to the course of steal syndrome in A/V fistulas (see *7), grafts even in stage II can improve, when venous anastomotic stenosis begins to reduce flow. These patients must be monitored not only for symptoms of their steal syndrome but also for access flow. When deterioration of graft function necessitates therapy, simultaneous treatment of steal syndrome is advised to prevent severe post-operative or post-interventional ischaemia.
*7 A/V fistula
• Once an A/V fistula causes stage II steal syndrome, further diagnostic assessment is indicated, and timely correction of steal syndrome should be done before progression to stage III or IV disease if objective assessment indicates reduction in perfusion pressure in the hand.
*8 Access compression and duplex ultrasound
• Steal syndrome occurs when there is diastolic retrograde inflow from the distal artery into the A/V fistula or graft. This phenomenon can easily be demonstrated by colour-coded duplex-sonography. Digital compression of the access without compression of the artery but complete blockade of access flow will return distal arterial flow direction to normal, thus improving peripheral circulation and usually return of distal pulses can be observed. Reactive hyperaemia is seen within seconds and can be detected by pulse oximetry, continuous transcutaneous pO2 (tcpO2) measurement, increase in the wrist brachial pressure index or digital photoplethysmography. 3 7 8
*9 Imaging : Upper limb arteriography
• Every patient with steal syndrome has to undergo thorough examination of his or her respective arm’s complete arterial tree 1 5 . After introducing an angiography catheter from the femoral or from the ipsilateral brachial artery via the Seldinger technique, all the arteries of the upper limb must be opacified from the ostium of the subclavian artery to the digital arteries. Due to the severely impaired arterial outflow, peripheral arteries can be sufficiently visualised (in most patients) only after digital compression of the access.
*10 Nerve conduction
• Ischaemic Monomelic Neuropathy (IMN). IMN leads to almost irreversible development of severe sensorimotor dysfunction distal to the arteriovenous anastomosis, sometimes without obvious tissue loss. IMN is thought to occur due to transient nerve ischaemia insufficient to cause tissue necrosis but resulting in severe nerve injury in susceptible patients (e.g. diabetics) 4.
• Waiting for the results of detailed nerve conduction studies must not lead to postponement of treatment in cases with unequivocal clinical signs and symptoms of IMN. Very urgent closure of the arteriovenous anastomosis is considered by many as the only way to avoid significant loss of sensomotor function.
*11 Interventional or surgical correction
• Central arterial stenoses (subclavian, axillary, brachial artery) proximal to the access can be dilated via the transfemoral route or in a retrograde fashion after cannulation of the access or of the brachial artery 5 7 9 10. The high arteriovenous flow seems to reduce the frequency of re-stenoses 9. If complete arterial occlusion cannot be reopened interventionally, standard vascular surgical bypass must be performed.