Arteriovenous Access – Revision

Measuring Access Function

Before the initiation of imaging or any intervention aimed at improving function, access failure must be detected. The most common measurement of access function is urea clearance with dialysis, or Kt/V, where K is the rate of clearance of urea, calculated from the pre- and postdialysis measurements; t is the duration of dialysis; and V is the patient's urea distribution volume. In this fashion, the “dose” of dialysis in a given session can be calculated objectively.

Access for dialysis affects the maximum dialysis dose in several ways. First, adequate flows in the access are needed for the dialysis machine to function efficiently. Currently, high-flow dialysis is the norm, with pump speeds of 350 mL/min or more. As long as the dialysis membranes can tolerate this high flow, the dose of dialysis can be given in a shorter time, reducing costs and resource use. Nonetheless, this high-flux technique requires much more efficient access function, with less tolerance of problems related to recirculation or high venous pressures. Recirculation, the re-treatment of blood already filtered by the dialysis machine, can be insidious, often showing up as poorer clearances with each subsequent dialysis treatment. Pressure limits are typically set on the dialysis machine; as a result, increasing venous pressures result in more prolonged dialysis owing to efforts to reposition the efferent needle and thus remedy the high pressures.

Mechanisms of Access Failure

Inadequate access function is related to flow limitation or problems with conduit access.

Flow Limitation

A perfectly functioning access needs adequate flows that exceed the pump speed of the dialysis machine by severalfold. With modern high-flux dialysis, pump speeds may approach 500 mL/min. Thus, flows of 1000 to 1200 mL/min are needed in the access to avoid recirculation. Additionally, adequate cardiac output is essential to maintain these flow rates. If cardiac output is marginal, decreased access flow may occur over the course of the dialysis session owing to decreased preload associated with successful fluid removal. Flow limitation results in the recirculation of already dialyzed blood to the dialysis machine, greatly limiting the effectiveness of dialysis.

Recirculation

Recirculation can result when the afferent needle pulls blood that has just been returned to the patient via the efferent needle. This partially dialyzed blood is then dialyzed a second time, with decreased removal of substrate owing to lower concentrations in the partially dialyzed blood. This results in a decreased effective dialysis dose, with a longer duration of dialysis required to achieve the same effectiveness. There are several mechanisms by which recirculation can occur.

Venous Outflow Stenosis.

The classic cause of recirculation is venous outflow stenosis, resulting in decreased flow through the access and increased recirculation of blood to the afferent needle. Regardless of the adequacy of arterial inflow, the outflow stenosis limits flow and increases recirculation. This is a common problem seen with AV grafts that are failing.

Arterial Inflow Stenosis.

Arterial inflow stenosis can similarly limit flow through the access, but in this case, both needles are distal to the stenosis. The limited arterial inflow results in recirculation from the distal efferent needle to the proximal afferent needle. This is a common mechanism of failure of autogenous AV access, occasionally leading to complete collapse of the outflow vein during dialysis.

Cannulation Location.

Another important cause of recirculation is poor needle cannulation separation. If the two needles for access can be placed sufficiently distant from each other, recirculation is unlikely, and dialysis can be effective even at low flow rates. Repeatedly puncturing at the same convenient location, rather than rotating puncture sites, can cause false aneurysms. If these are sufficiently large, recirculation can occur owing to stagnant flow within the aneurysm rather than limited flow within the access. These false aneurysms are problematic because they are often the sites of infiltration and bleeding ( Figure 80-1-3 ).

Causes of Access Failure

Once dialysis access is achieved, the mode of failure is usually related to the type of access constructed. For catheters, function is often decreased over time by clots or fibrin sheaths. For both autogenous and prosthetic accesses, the issue is often the development of venous outflow stenosis or stenosis of the autogenous access itself, leading to limited clearance. Autogenous accesses have limited patency after thrombectomy, so intervention is recommended before thrombosis can occur. Prosthetic grafts thrombose at a higher overall flow rate than autogenous accesses, but they have better patency after thrombectomy. Often, prosthetic grafts can fail multiple times before abandonment of the access must be considered. The underlying cause of stenosis in AV access is intimal hyperplasia (IH).

IH is the greatest unsolved problem in hemodialysis. Although IH can occur anywhere in the outflow veins used for access, certain anatomic factors predispose to local or remote stenoses. For example, central venous stenosis is common in both autogenous and prosthetic AV accesses ( Figure 80-1-4 ). In the past, this was often blamed on the use of subclavian catheters, because the subclavian veins were the most common sites of central venous access. In most modern dialysis centers, use of the subclavian veins for catheter access is avoided for this reason; yet a high incidence of subclavian vein stenosis is still associated with upper extremity dialysis access. It is likely that the high flow across the subclavian vein at the thoracic inlet generates turbulence that leads to IH and stenosis. In this fashion, almost any vein used in the outflow of an AV access can develop IH and stenosis. Another unavoidable factor is puncture of the conduit, which leads to IH in autogenous conduits and to local tissue ingrowth, simulating IH in prosthetic grafts. Finally, IH occurs at AV access anastomoses, aggravated by excess turbulence compared with arterial-arterial anastomoses.

Detection of Access Failure