NKF KDOQI GUIDELINES
I. CLINICAL PRACTICE GUIDELINES FOR VASCULAR ACCESS
GUIDELINE 6. TREATMENT OF ARTERIOVENOUS GRAFT COMPLICATIONS
Appropriate management and treatment of AVG complications may improve the function and longevity of the vascular access.
6.1 Extremity edema:
Patients with extremity edema that persists beyond 2 weeks after graft placement should undergo an imaging study (including dilute iodinated contrast) to evaluate patency of the central veins. The preferred treatment for central vein stenosis is PTA. Stent placement should be considered in the following situations:
- 6.1.1 Acute elastic recoil of the vein (>50% stenosis) after angioplasty. (B)
- 6.1.2 The stenosis recurs within a 3-month period. (B)
6.2 Indicators of risk for graft rupture:
Any of the following changes in the integrity of the overlying skin should be evaluated urgently:
- 6.2.1 Poor eschar formation. (B)
- 6.2.2 Evidence of spontaneous bleeding. (B)
- 6.2.3 Rapid expansion in the size of a pseudoaneurysm. (B)
- 6.2.4 Severe degenerative changes in the graft material. (B)
6.3 Indications for revision/repair:
- 6.3.1 AVGs with severe degenerative changes or pseudoaneurysm formation should be repaired in the following situations:
- 126.96.36.199 The number of cannulation sites are limited by the presence of a large (or multiple) pseudoaneurysm(s). (B)
- 188.8.131.52 The pseudoaneurysm threatens the viability of the overlying skin. (B)
- 184.108.40.206 The pseudoaneurysm is symptomatic (pain, throbbing). (B)
- 220.127.116.11 There is evidence of infection. (B)
- 6.3.2 Cannulation of the access through a pseudoaneurysm must be avoided if at all possible and particularly so if the pseudoaneurysm is increasing in size. (B)
6.4 Treatment of stenosis without thrombosis:
Stenoses that are associated with AVGs should be treated with angioplasty or surgical revision if the lesion causes a greater than 50% decrease in the luminal diameter and is associated with the following clinical/physiological abnormalities:
- 6.4.1 Abnormal physical findings. (B)
- 6.4.2 Decreasing intragraft blood flow (<600 mL/min). (B)
- 6.4.3 Elevated static pressure within the graft. (B)
6.5 Outcomes after treatment of stenosis without thrombosis:
After angioplasty or surgical revision of a stenosis, each institution should monitor the primary patency of the AVG. Reasonable goals are as follow:
- 6.5.1 Angioplasty:
- 18.104.22.168 The treated lesion should have less than 30% residual stenosis and the clinical/physiological parameters used to detect the stenosis should return to acceptable limits after the intervention. (B)
- 22.214.171.124 A primary patency of 50% at 6 months. (B)
- 6.5.2 Surgical revision:
- 126.96.36.199 The clinical/physiological parameters used to detect the stenosis should return to acceptable limits after the intervention. (B)
- 188.8.131.52 A primary patency of 50% at 1 year. (B
6.6 If angioplasty of the same lesion is required more than 2 times within a 3-month period, the patient should be considered for surgical revision if the patient is a good surgical candidate.
- 6.6.1 If angioplasty fails, stents may be useful in the following situations:
- 184.108.40.206 Surgically inaccessible lesion. (B)
- 220.127.116.11 Contraindication to surgery. (B)
- 18.104.22.168 Angioplasty-induced vascular rupture. (B
6.7 Treatment of thrombosis and associated stenosis:
Each institution should determine which procedure, percutaneous thrombectomy with angioplasty or surgical thrombectomy with AVG revision, is preferable based upon expediency and physician expertise at that center.
- 6.7.1 Treatment of AVG thrombosis should be performed urgently to minimize the need for a temporary HD catheter. (B)
- 6.7.2 Treatment of AVG thrombosis can be performed by using either percutaneous or surgical techniques. Local or regional anesthesia should be used for the majority of patients. (B)
- 6.7.3 The thrombectomy procedure can be performed in either an outpatient or inpatient environment. (B)
- 6.7.4 Ideally, the AVG and native veins should be evaluated by using intraprocedural imaging. (B)
- 6.7.5 Stenoses should be corrected by using angioplasty or surgical revision. (B)
- 6.7.6 Methods for monitoring or surveillance of AVG abnormalities that are used to screen for venous stenosis should return to normal after intervention. (B)
6.8 Outcomes after treatment of AVG thrombosis:
After percutaneous or surgical thrombectomy, each institution should monitor the outcome of treatment on the basis of AVG patency. Reasonable goals are as follows:
- 6.8.1 A clinical success rate of 85%; clinical success is defined as the ability to use the AVG for at least 1 HD treatment. (B)
- 6.8.2 After percutaneous thrombectomy, primary patency should be 40% at 3 months. (B)
- 6.8.3 After surgical thrombectomy, primary patency should be 50% at 6 months and 40% at 1 year. (B)
6.9 Treatment of AVG infection:
Superficial infection of an AVG should be treated as follows:
- 6.9.1 Initial antibiotic treatment should cover both gram-negative and gram-positive microorganisms. (B)
- 22.214.171.124 Subsequent antibiotic therapy should be based upon culture results.
- 126.96.36.199 Incision and drainage may be beneficial.
- 6.9.2 Extensive infection of an AVG should be treated with appropriate antibiotic therapy and resection of the infected graft material. (B
In this update of the KDOQI Guidelines, the Work Group did not perform a comprehensive literature and data review of recent studies of AVG complications. The primary change from previous versions of the KDOQI Vascular Access Guidelines is consolidation of related material on AVGs into a single unified guideline. However, the fundamental tenets are unchanged from previous editions. Newer references, including reviews, are included when appropriate.
Extremity Edema and Stenosis (CPG 6.1)
The AVG, although decreasing in frequency of use, remains a major type of vascular access for HD in the United States.2 The natural history of an AVG is the progressive development of neointimal hyperplastic stenoses in the outflow track. Although these stenotic lesions most commonly occur at the venous anastomosis, they also can occur at the arterial anastomosis and within the native veins that provide outflow from the AVG. This resulting increase in venous pressure leads to edema proximally and, in extreme circumstances, evidence of venous collateral flow. The presence of a hemodynamically significant stenosis can decrease the ability of the access to deliver adequate flow and increase the risk for AVG thrombosis. Early detection and treatment of hemodynamically significant stenoses is considered a primary tenet of a vascular access management program.
Extremity edema persisting beyond 2 weeks (immediate postoperative period) after placement of an AVG may indicate inadequate venous drainage or central venous obstruction.30,436 In many cases, the stenosis results from the prior placement of a subclavian catheter; risk for stenosis is increased by previous catheter infection.170 PTA of the stenotic or obstructed venous segment can lead to resolution of the edema. However, acute elastic recoil may occur after angioplasty of large central veins.437 Studies have shown that the use of stents may improve long-term patency of the central vein in certain circumstances.438-442 Surgical treatment of central venous stenosis is associated with substantial morbidity and should be reserved for extraordinary circumstances.443
Graft Degeneration and Pseudoaneurysm Formation (CPG 6.2, CPG 6.3)
Repeated cannulation of an AVG may cause degeneration of the graft material that can progress to involve the subcutaneous tissues overlying the vascular access.444,445 These degenerative changes may eventually compromise the circulation to the skin. Degeneration of the AVG and necrosis of the overlying subcutaneous tissue may lead to a progression of clinical problems, including difficulty achieving hemostasis upon needle withdrawal, spontaneous bleeding from cannulation sites, severe hemorrhage, and—ultimately—acute graft rupture. The degeneration of AVGs combined with a venous outflow stenosis fosters formation of a pseudoaneurysm. Progressive enlargement of a pseudoaneurysm produces thinning of the overlying skin, thereby accelerating skin necrosis that increases the risk for acute graft rupture. A large pseudoaneurysm can limit the availability of needle cannulation sites. Dialysis needles must not be inserted into a pseudoaneurysm. A severely degenerated graft or enlarging pseudoaneurysm should be repaired to decrease the risk for acute rupture and restore additional surface area for cannulation.
A pseudoaneurysm is treated most effectively by resection and segment interposition.106,446 Pseudoaneurysms that are not resected may expand and rupture, resulting in significant blood loss. Pseudoaneurysms that exceed twice the diameter of the graft or those that are increasing in size should be surgically corrected because of their increased risk for rupture. At times, an endovascular covered stent option may exist.447 Pseudoaneurysm expansion that threatens the viability of the skin places the patient at risk for graft infection. In these cases, surgical correction is indicated.
Treatment of Stenoses (CPG 6.4-6.8)
Venous stenosis is the most common lesion in AVGs, although in many cases, more than 1 lesion is present within the graft or at the anastomoses. Although previous studies suggested that arterial inflow lesions were uncommon (<5% of all lesions),108,266 more recent experience suggests the arterial or arterial anastomotic lesion affecting blood flow into the AVG may be up to 20% to 25% of all lesions identified by angiography.
A hemodynamically significant outflow stenosis decreases intragraft blood flow and increases intragraft pressure.10 The lower blood flow, in turn, may reduce the efficiency of HD treatment327,355 and increase the risk for vascular access thrombosis.285,287,322,340,347,364,376,448,449 Conversely, inflow lesions and intragraft lesions may be associated with low pressure in the body of the graft and venous outflow. A hemodynamically significant stenosis is defined as a 50% or greater reduction in normal vessel diameter accompanied by a hemodynamic, functional, or clinical abnormality (see CPG 4).449,450 By means of angiography, about 90% of thrombosed grafts are associated with stenosis, predominantly in the outflow, at the venous anastomosis, and more centrally.109,110,451,452
PTA or surgical repair of a hemodynamically significant stenosis associated with a nonthrombosed AVG can maintain functionality and delay thrombosis of the vascular access.269,453,454 Many nonrandomized trials have shown that preemptive treatment of stenoses reduces the rate of thrombosis10,322,374,455 and perhaps prolongs the useful life span of the AVG.10, 322, 374 A number of observational, but not randomized, studies show that a greater fraction of grafts remain free of interventions or thrombosis if the AVG is patent at the time of intervention.111,112,269,354,456 The fraction of AVGs free of further intervention or thrombosis ranged from 71% to 85% among 4 studies if PTA was performed preemptively compared with only 33% to 63% if PTA was performed after thrombectomy of the graft.10,322,374,455
Although these results would suggest that elective correction of stenoses before thrombosis might increase the long-term survival of the AVG, recent studies suggested that prophylactic treatment of stenoses, although reducing thrombosis events, does not extend the useful life span of AVG rates.384,386 Thus, the major reason for surveillance is the prevention of thrombosis (see CPG 4).
No convincing evidence exists showing that repair of an asymptomatic anatomic stenosis (>50% diameter reduction) improves function or delays thrombosis of the vascular access. Therefore, prophylactic treatment of a stenosis that fulfills the anatomic criteria (>50% diameter reduction), but is not associated with a hemodynamic, functional, or clinical abnormality, is not warranted and should not be performed.10,322,354
Arterial stenosis associated with diminished access inflow and frequently suspected by the presence of excessively negative dialysis circuit prepump pressures (arterial tubing to pump) should be evaluated and corrected when found.
After PTA, anatomic success is defined as residual stenosis less than 30%.20,457 Published series have consistently reported a 6-month primary (unassisted) patency rate of 40% to 50% after PTA of stenoses associated with nonthrombosed AVGs.108,111,112,269,354,456 The expected primary patency rate after surgical repair of stenoses associated with nonthrombosed grafts is less well established.458 Previous Vascular Access Work Groups have determined that a 1-year primary patency rate of 50% after surgical revision should be the goal.
Individual patients may have a rapid recurrence of stenoses that requires repeated PTA.108,453 In these patients, repeated angioplasty may not be cost-effective, and surgical revision may be beneficial. Previous Vascular Access Work Groups have defined rapid recurrence of a stenosis as the need for more than 2 angioplasty procedures within a 3-month interval.
Previous studies reported that the use of endovascular stents as the primary treatment for venous stenosis provides long-term results that are similar to those obtained with angioplasty alone.382,459-461 Stents should be reserved for patients with contraindications to surgical revision and for treatment of angioplasty-induced venous rupture.462-464
Several studies have directly compared percutaneous thrombectomy with surgical thrombectomy with revision for treatment of AVG thrombosis.465-470 A review of comparative and noncomparative studies reveals conflicting results and does not yield a definitive preference.24,106,356,467-479 In the opinion of the Work Group, percutaneous thrombectomy or surgical thrombectomy with revision are both effective techniques for the treatment of AVG thrombosis and associated stenosis. The thrombectomy procedure should be performed expeditiously to avoid the need for a short-term catheter. Hospitalization and general anesthesia increase the cost and risk of the thrombectomy procedure and should be avoided when possible.
An underlying stenosis frequently (>85%) is the cause of AVG thrombosis.108,480,481 Intraprocedural imaging should be used to evaluate the outflow veins for improved detection of significant stenoses.382,470 Identification and treatment of all significant stenoses are essential to optimize long-term patency of the thrombectomy procedure. PTA of stenoses associated with AVG thrombosis correlates with poorer outcomes compared with nonthrombosed AVGs.269 After percutaneous thrombectomy, the majority of reported 3-month primary (unassisted) patency rates range from 30% to 40%.471,473,476,478,480,481 The Work Group believes that percutaneous thrombectomy should achieve a 3-month primary patency rate of 40%. After surgical thrombectomy, the achievable goals are a 6-month primary patency rate of 50% and a 1-year primary patency rate of 40%. Surgical procedures are held to a higher standard because the AVG usually is extended farther up the extremity when a surgical revision of a stenosis is performed, using up “venous capital.”
Infection (CPG 6.9)
While cardiac causes account for almost half the deaths in adult patients with CKD stage 5, the second leading cause of death is infection, much of it related to the type of vascular access in use.60 AVGs have a greater rate of infection than autologous fistulae, and, unfortunately, antibiotics alone frequently are inadequate and surgical procedures are needed.482 Management of an AVG infection is a balance between achieving resolution of the infection while preserving the vascular access.59,483 Superficial infections should be treated initially with broad-spectrum antibiotic therapy. Subsequent antibiotic therapy should be based upon the identification of the causative bacterial organism.201,484 A more extensive AVG infection can lead to bacteremia, sepsis, and death. Surgical exploration and removal of infected graft material, combined with antibiotic therapy, often is necessary for complete resolution.484
Subclinical infection can develop in AVGs, typically resulting from retained graft material. Diagnosis may require performance of indium-labeled white blood cell or gallium scans. Such infection frequently is manifested as resistance to epoetin therapy, along with evidence of a systemic inflammatory response; frequently, it occurs in abandoned and nonfunctioning grafts. Epoetin responsiveness is restored only after removal of the graft.
LIMITATIONS AND COMPARISON TO OTHER GUIDELINES
These updated CPGs are essentially unchanged in content from those of previous editions of the KDOQI Vascular Access Guidelines. More evidence now is available for the guidelines than in previous editions. However, there is still a paucity of RCTs to better define the effect of interventions on clinically important outcomes. These guidelines also are comparable to those recommended by the Society of Interventional Radiology,457 American College of Radiology,485 and a joint committee of several surgical societies.458
|© 2006 National Kidney Foundation, Inc.|