**8. Arteriovenous graft complications**

AVGs have a functional life much shorter than AVFs. Neointimal hyperplasia causes venous stenosis, which leads to thrombosis, and this is the natural course of AVGs. The principal cause of thrombosis is the increased production of smooth muscle cells, myofibroblasts and vascu‐ larization within the neointima. Around the graft, there is also angiogenesis and numerous macrophages in the tissue [210, 211]. Growth factors (GF) such as VEGF (vascular endothelial), PDGF (platelet derived) and basic FGF (fibroblast) are present within the neointimal lesion [211]. The presence of shear stress regulates vascular endothelium [212, 213] and that flow within AVGs is likely to be different from native veins. Understanding the pathophysiology of neointimal hyperplasia could lead to targeted therapy. Current studies are evaluating the role of radiation [214], decoy peptides against transcription factors [215, 216] and local delivery of drugs with cell-cycle inhibitory effects (e.g., paclitaxel [217] and sirolimus). Cell-based strategies seek to take advantage of endothelial progenitor cells that release endogenous inhibitors of proliferation and thrombosis, such as nitric oxide (NO) and prostacyclin [218]. Venous stenosis in AVGs leads to decreased blood flow and thrombosis, at a rate of 1–1.5 times/ patient/year [70]. Thrombosis is associated with anatomical stenosis, in most cases, which is located in the venous anastomosis (60%), followed by the peripheral vein (37%) and within the graft (38%) [219]. Stenosis and closure by venous anastomoses are the most frequent causes of failure of AVG for hemodialysis. AVG closure can be addressed surgically and endovasc‐ ularly (amenable to thrombectomy by radiological or surgical means) [220]. Percutaneous angioplasty is safe and effective in treating venous stenosis [221], with a success rate of 80% to 94% and primary patency around 60% at 6 months and 40% at 1 year. The placement of selfexpanding nitinol stents at the venous anastomosis appears to prolong patency in cases where focal lesions are resistant to repeated angioplasty and recur and improve PTFE grafts longevity in selected cases of older grafts [222]. Central stenosis is technically more difficult to treat, and stenotic lesions often recur within 6 months [77]. Recently, a modular anastomotic valve device (MAVD) has been in preliminary use in order to isolate the graft from the circulation between dialysis sessions, decreasing the flow disturbances this way and as a result the intimal hyperplasia [223]. During the last decades, percutaneous techniques became increasingly important for the treatment of AVG failure [224]. Cutting balloon angioplasty is a safe and effective treatment of graft to vein anastomotic stenosis, with significantly higher patency than that of conventional balloon angioplasty [225]. From the point of view of Troisi et al. [226], the combined simultaneous hybrid (open and endovascular) approach in urgency maximizes the use of different available techniques, improving overall success rate to save a thrombosed graft.

As described above, AVGs' thromboses are usually the result of multiple factors; such as stenosis, hypotension and excessive compression for hemostasis. Hemodialysis nurses have to be careful in order to avoid these factors. Thrombosis risk increases as blood flow (BF) decreases, as May et al. [227] showed in their study. AVG thrombosis can be managed in an outpatients' basis endovascularly. Angiography for venous stenosis is always required and is often accompanied by an angioplasty.

**Figure 14.** Aneurysm in forearm AVF.

262 Updates in Hemodialysis

Infections of AVFs are rare but must be treated properly due to patients' impaired immuno‐ logic status. Very rare infections of the AV anastomosis require surgery with resection of the infected tissue. More often, infections occur at cannulation sites and then the arm should be rested and cannulation cease [208]. In all cases of AVF infection, antibiotic therapy is initiated with broad-spectrum vancomycin plus an aminoglycoside and converting to appropriate one based on results of culture and sensitivities. Infections of primary AVFs should be treated for

AVGs have a functional life much shorter than AVFs. Neointimal hyperplasia causes venous stenosis, which leads to thrombosis, and this is the natural course of AVGs. The principal cause of thrombosis is the increased production of smooth muscle cells, myofibroblasts and vascu‐ larization within the neointima. Around the graft, there is also angiogenesis and numerous macrophages in the tissue [210, 211]. Growth factors (GF) such as VEGF (vascular endothelial), PDGF (platelet derived) and basic FGF (fibroblast) are present within the neointimal lesion [211]. The presence of shear stress regulates vascular endothelium [212, 213] and that flow within AVGs is likely to be different from native veins. Understanding the pathophysiology of neointimal hyperplasia could lead to targeted therapy. Current studies are evaluating the role of radiation [214], decoy peptides against transcription factors [215, 216] and local delivery of drugs with cell-cycle inhibitory effects (e.g., paclitaxel [217] and sirolimus). Cell-based strategies seek to take advantage of endothelial progenitor cells that release endogenous inhibitors of proliferation and thrombosis, such as nitric oxide (NO) and prostacyclin [218]. Venous stenosis in AVGs leads to decreased blood flow and thrombosis, at a rate of 1–1.5 times/ patient/year [70]. Thrombosis is associated with anatomical stenosis, in most cases, which is located in the venous anastomosis (60%), followed by the peripheral vein (37%) and within the graft (38%) [219]. Stenosis and closure by venous anastomoses are the most frequent causes of failure of AVG for hemodialysis. AVG closure can be addressed surgically and endovasc‐

a total of 6 weeks, analogous to subacute bacterial endocarditis [209].

**8. Arteriovenous graft complications**

Prompt pharmaceutical thrombolysis or mechanical removal of the thrombus with a Fogarty catheter and thromboaspiration or thrombectomy with a mechanical device [228] may avoid a new catheter placement.

Infections of AVGs are severe complications and the second cause of vascular access loss. Hemodialysis-related bacteraemia is 10-fold more often in AVGs than AVFs: 2.5 incidents every 1000 HD sessions versus 0.2 [229]. It seems that the most significant modifiable risk factor is patients' hygiene [230].

A referral to surgeon of pseudoaneurysms for resection is imposed when they are increasing rapidly in size, their width is more than 2-fold bigger than the graft, or the overlying skin seems under duress (thin, bleeding, blanching) [231].

Ischemia, as a result of access placement, is more common for AVGs than AVFs: vascular steal syndrome and ischemic monomelic neuropathy are two important clinical entities to distin‐ guish.

"Physiological" steal phenomenon occurs in 73% of AVFs and 90% of AVGs. Thus, in a radiocephalic fistula, arterial blood from the palmar arch may also deliver blood into the fistula. Unless there is the capacity for collateralization, this can lead to ischemia in the hand, ranging from complaints about cold hands to necrotic fingertips. Most of these complaints improve over time, but 1% of AVFs and up to 4% of AVGs require surgical revision [232]. Doppler ultrasonography is a useful adjunctive tool to determine the etiology of chronic hemodialysis access-induced distal ischemia (HAIDI). Conservative measures combined with close follow-up can be used as the first step in the management of chronic HAIDI patients with mild symptoms [233]. Ischemic monomelic neuropathy is characterized by warm hands with a good pulse, but the hands are tender and swollen, usually immediately after surgery, and there is muscle weakness [234]. The cause is likely ischemia of the nerves, and rapid surgical reevaluation is needed. Wound and skin complications and greater incidence of thrombosis of VA associated with recombinant human erythropoietin have been reported (rHuEPO) [235].
