Arteriovenous endovascular fistula is the preferred vascular access for hemodialysis patients at home and abroad, and it is the “lifeline” for hemodialysis patients by providing adequate blood flow and smooth dialysis. The care of the endovascular fistula is actually the treasure of the life of the hemodialysis patient, and the arteriovenous endovascular fistula stenosis has become a major cause of thrombosis and occlusion; therefore, K/DOQI recommends routine monitoring and maintenance of the arteriovenous endovascular fistula, early detection and intervention of the arteriovenous endovascular fistula stenosis in order to prolong its service life.
I. Definition and typing of non-thrombotic stenosis in arteriovenous endovascular fistulae
There is no exact definition of arteriovenous stenosis, but if the diameter of the stenotic vessel is >50% of the diameter of the adjacent fistula, it is considered to have anatomical stenosis, while clinically arteriovenous stenosis has hemodynamic changes, such as decreased dialysis blood flow, increased venous pressure, increased access recirculation and abnormal physical examination. Type I stenosis is anastomotic stenosis, which is located at or immediately adjacent to the anastomosis; type II stenosis is stenosis at the puncture site, which includes the following two conditions: a shorter stenosis at the puncture site or stenosis of the vein between the two puncture sites, and multiple or longer stenoses at the puncture site; type III stenosis is stenosis at the vascular confluence, which mainly refers to stenosis at the confluence of the vessels in the upper arm endovascular fistula. Mostly seen in brachial cephalic endovascular fistula, the stenosis is located at the confluence of cephalic and axillary veins stenosis.
Causes of non-thrombotic stenosis in arteriovenous fistula
The causes of non-thrombotic stenosis in arteriovenous endovascular fistulae are mainly the following
1.Intimal hyperplasia
Increased expression of α-smooth muscle actin, proliferation of smooth muscle cells and myofibroblasts, increased extracellular matrix components, formation of endothelial and epithelial neovascularization, and involvement of inflammatory cells, cell regulatory proteins and cytokines are the main mechanisms leading to endothelial hyperplasia. Endothelial injury is the initiating factor leading to endothelial hyperplasia. The main factors leading to endothelial injury are: (1) surgical trauma during endovascular fistuloplasty; (2) endovascular hemodynamic changes: endovascular fistuloplasty can cause changes in the shear force of the anastomosis and endovascular arteriovenous wall. (3) Dialysis puncture: Ju-Feng et al. applied ultrasound technique to observe the effect of puncture on endovascular fistula and found that puncture can cause vasodilatation and intimal thickening of arteriovenous endovascular fistula. (4) Endothelial damage caused by angioplasty treatment: Although angioplasty is a treatment method, the treatment process can cause serious damage to the endothelium and smooth muscle cells, exacerbating the occurrence of restenosis. chang et al. confirmed that the degree of cell proliferation was significantly increased in endovascular fistula stenosis treated by angioplasty compared with the initial stenosis. (5) Vascular endothelial dysfunction caused by uremic toxins: Patients with uremia are in a long-term microinflammatory state, and inflammation and oxidative stress can cause vascular endothelial damage, promote vascular smooth muscle cell migration, and participate in the endothelial proliferation process.
2.Improper puncture
Repeated puncture of the same site or confined to a small section of the vein causes damage to the vein wall and endothelial thickening, in addition to improper puncture can cause hematoma, hematoma mechanization compression causes endovascular stenosis and thrombosis.
3.Improper compression
Improper compression and hemostasis after dialysis or too tight bandages lead to hemodynamic changes and segmental dilatation and narrowing of the vessel wall.
4.Drug stimulation and infection
Superficial thrombophlebitis caused by drug injection or infusion in the vein on the side of arteriovenous endovascular fistula, resulting in intimal hyperplasia, narrowing of the lumen, slow blood flow and thrombosis.
5.Other
Stenosis is caused by the accumulation of mechanized laminar clots in the graft vessel or repeated punctures resulting in inward growth of fibrous tissue covering the inner wall of the artificial vessel.
Diagnosis of non-thrombotic stenosis of arteriovenous endovascular fistula
Arteriovenous stenosis can be diagnosed when the internal diameter of the arteriovenous fistula is >50% of the diameter of the adjacent fistula, when there is an increase in venous pressure during dialysis, when there is a decrease in blood flow in the vascular access, when there is an increase in the recirculation rate in the vascular access, when there is swelling in the limb on the side of the arteriovenous fistula, and when there is an unexplained decrease in the efficiency of dialysis.
IV. Treatment of non-thrombotic stenosis of arteriovenous fistula
The treatment of non-thrombotic stenosis of arteriovenous endovascular fistula includes interventional treatment and surgical treatment.
PTA treatment has the advantages of less trauma, higher safety, less vascular damage, relatively less complications, higher immediate opening rate, and maximum preservation of available vessel length, etc. The indications for treatment are that PTA or surgical treatment should be performed if the arterial inlet or venous outflow tract stenosis exceeds 50%, accompanied by clinical or physiological abnormalities, which include: decreased blood flow, elevated static venous pressure, and PTA should be performed using a cis-puncture approach if the stenosis is far from the endovascular anastomosis and a retrograde puncture approach if the stenosis is close to the endovascular anastomosis; the diameter of the balloon should be equal to or 1 mm larger than the diameter of the adjacent normal vessel or graft, unless the vessel is unusually small, in which case a 6-8 mm diameter balloon is generally used for dialysis endovascular fistulas. A pressure of 10-12 standard atmospheres (atm) can be used for most stenoses. For tough endovascular stenoses, high-pressure balloons rated at 20 standard atmospheres (atm) of burst pressure, such as the Boston Scientific Blue Max balloon rated at 20 atm or the Bard Conquest balloon rated at 30 atm, may be used. Alternatively, a cutting balloon may be used. residual stenosis should be <30% after PTA treatment, indicating that the clinical/physiological parameters of the stenosis have returned to an acceptable range.
2. Stent placement may be considered in cases where transangioplasty has failed and there is no suitable alternative site for the creation of an arteriovenous endovascular fistula or where surgical management is difficult or contraindicated.
3.Surgery is the most thorough method for the treatment of arteriovenous endovascular stenosis, which can minimize the recurrence rate of stenosis. The surgical approach is to operate end-to-end, end-to-side or side-to-side anastomosis of the arteriovenous vein proximally above the site of stenosis occurrence, with an anastomotic diameter of 5-8 mm; for patients with stenosis or embolism of the entire forearm, a high endovascular fistula is established; vascular grafts and bypasses can also be performed.