This July issue of Vascular Disease Management has interesting articles, each worthy of editorial comment. I have chosen to comment on Dr. Bak’s article on “Endovascular Therapies for Hemodialysis Access.” The incidence of hemodialysis is increasing worldwide, despite improvement in hypertensive therapy, as people are living longer, and there is an epidemic of diabetes. Patients on hemodialysis are living longer with improved medical care increasing time on dialysis. Increased utilization of diagnostic and therapeutic procedures with iodinated contrast media may also be causal of acute renal failure or serve as the dialysis-precipitating events for patients with pre-existing chronic kidney disease (CKD). Great strides have been made in dialysis therapy. Hemodialysis can be performed in less time, with improved efficiency, as compared to prior treatments. Hemodialysis is lifesaving for patients with acute kidney disease and CKD.
Adequate access is often the limiting factor in delivering this therapy over prolonged time periods in chronic renal failure. An arteriovenous (AV) fistula is the most durable access for chronic therapy. These are often not placed early enough for maturation prior to hemodialysis, necessitating placement of temporary catheters or AV grafts, which have a shorter life expectancy and may take away a future fistula option at that site. Unfortunately, even mature grafts and fistulae have a short useful lifespan and frequently fail without appropriate interventions to keep them functional. Arterial inflow, venous outflow, fistula size, compression protocols, and degree of thrombogenicity affect graft patency and longevity. Appropriate surveillance and intervention can salvage grafts that are not maturing properly, as well as maintain failing functional grafts.
Arteriovenous fistulae fail if there is inadequate arterial inflow, intimal hyperplasia at the site of AV anastamosis or within the proximal “arterialized” venous segment, central venous obstruction, venous collaterals limiting venous graft enlargement, and thrombosis that can be related to compression protocols and hyperthrombogenicity. Because diabetes is the most common etiology of CKD, diffuse arterial disease, particularly in distal vessels, is common. Dystrophic arterial calcification is routinely present in CKD patients, potentially hindering ideal AV anastomosis creation and making arterial intervention more difficult. Arterial inflow is crucial for a properly functioning fistula and for blood supply to tissues distal to the graft. Increased flow through the graft can potentially result in cardiac decompensation in patients with impaired cardiac output, as well as distal tissue loss if there is distal PAD. Loss of functioning radial arteries from radial access catheterization attrition and from harvest for use as bypass conduits may reduce access options. Venous outflow is crucial. Iatrogenically induced central venous stenosis and obstruction are more common with increased utilization of indwelling central lines as well as electrophysiological devices, which often have multiple leads that may obstruct veins. Intimal hyperplasia at the AV anastomosis is common. These strictures are often difficult to dilate, frequently requiring high-pressure noncompliant balloons.
Because of the short natural lifespan of AV fistulae, many patients have historically run out of access options during prolonged chronic hemodialysis therapy. Bak has clearly presented that better management of access sites may salvage sites that were historically abandoned, prolong the effective life of the access sites, save money, and prevent complications (there is risk of limb ischemia and embolization if declotting is required and there is intrinsic risk and cost with new fistula creation).
Perhaps drug-eluting balloons, drug-eluting stents, better stent designs, scoring and high-pressure balloons, devices that allow more effective treatment of calcified lesions, and stent grafts will improve interventionists’ abilities to preserve fistula function and increase their useful life by decreasing restenosis and occlusion. Identifying dysfunctional fistulae at early stages, when therapy is less dangerous (embolic risk) and has greater chance of success, is crucial. Careful planning to lessen chances of radial and brachial artery injury and limit central venous stenosis must be considered in all patients with impaired renal function long before dialysis is contemplated. This will require the coordinated efforts of invasive cardiologists, electrophysiologists, interventional radiologists, vascular surgeons, and oncologists, if we are to preserve access options.