Fig. 33.1
Arteriovenous fistula aneurysms classification by Valenti and colleagues
Type 1a: The vein uniformly aneurysmal from the arterial anastomosis along most, if not all, of its length resembling a hosepipe (Fig. 33.2).
Fig. 33.2
Diffuse aneurysmal degeneration of a right brachiobasilic arteriovenous fistula. The vein is uniformly aneurysmal from the arterial anastomosis of the entire length of the arteriovenous fistula resembling a hosepipe
Type 1b: The proximal part of the vein is dilated within 5 cm of the arterial anastomosis.
Type 1 AVF aneurysms were most common in unused AVF and appeared to be associated with high-flow states.
Type 2a: The classic “camel hump” with at least one localized area of dilation. These areas of dilation correlate with sites of access needle placement for hemodialysis. In between these localized aneurysms, the vein is of normal caliber or has stenosis (Fig. 33.3).
Fig. 33.3
Left brachiocephalic arteriovenous fistula with large bilobed aneurysmal degeneration creating a challenge for needle placement and complicated by progressive skin thinning. (a) Anterior view. (b) Lateral view
Type 2b: There is both a post-anastomotic aneurysm and also multiple aneurysmal segments throughout the length of the vein; thus, it is a combination of types 1b and 2a.
Type 2 AVF aneurysms are more common in AVF being used for hemodialysis.
Type 3: Complex/heterogeneous. This was the minority of AVF aneurysms (3.7 %) that did not fit into any typical pattern.
Type 4: These may appear as aneurysms, but on duplex they are found to be pseudoaneurysms and thus are indistinguishable from type 2 AVF aneurysms on clinical exam.
The Balaz Classification System
This classification is based on ultrasound or fistulagram findings as follows:
Type I: Without stenosis and thrombosis.
Type II: With hemodynamic significant stenosis (≥50 %), this is further subdivided by location of the stenosis: (A) in the inflow artery, (B) in the at arterial anastomosis, (C) along the cannulation zone, and (D) in the central vein.
Type III: With partial thrombosis occluding ≥50 % of the lumen.
Type IV: With complete thrombosis of the AVF.
Pathophysiology
Formation of an AVF aneurysm starts at the time of the creation of the AVF. The combination of a low venous outflow resistance and venous wall distention leads to venous wall remodeling into an arterialized vein. The vein over time dilates and becomes tortuous because of the constant arterial pressure. As the vein dilates and the diameter enlarges, the wall tension increases, causing further vein dilation [2].
Several mechanisms have been proposed to explain the pathophysiology of AVF:
Central or outflow vein stenosis: the increased venous pressure due to the central veins and outflow vein stenosis accelerates the aneurysmal degeneration (Fig. 33.4). In a detailed study of 89 patients with AVF aneurysms at a mean diameter of 2.3 cm, 78 % had an associated venous outflow stenosis. The stenoses were present most commonly in the outflow cephalic vein (57 %), followed by the cephalic arch (20 %), brachiocephalic vein (10 %), and subclavian vein (6 %) [8]. Outflow stenoses in AVFs with aneurysmal degeneration were observed in 87 % of brachiocephalic AVFs, 60 % of radiocephalic AVFs, and 80 % of brachiobasilic AVFs [8]. Central venous stenosis was documented in 90 % of cases in two series of AVF aneurysms requiring surgical revision [9, 10].
Fig. 33.4
A patient with a left brachiocephalic arteriovenous fistula with aneurysmal degeneration due to central venous stenosis. (a) Note the collaterals on the left side of the chest and neck. (b) Diagnostic fistulagram showing near occlusion of the innominate artery and reflux in the left internal jugular vein. Of note, the patient was experiencing headaches during his hemodialysis treatment. (c) Treatment of the stenosis by balloon angioplasty. The patient’s headaches resolved after treatment. (d) Circumferentially dissected arteriovenous fistula with an overlying skin island. (e) The aneurysm treated with excision and end-to-end anastomosis of the remainder of the fistula
Repeated punctures at clustered sites. Repeated needling results in multiple small fibrous scars in the vessel wall, which may expand with time and result in localized aneurysmal areas (Fig. 33.5) [2]. This can occur due to two different mechanisms, repeated trauma causes thinning of the wall of the AVF and aneurysm formation or repeated trauma leads to an area of stenosis causing pre- or post-stenotic aneurysmal degeneration [4]. It can be difficult at time to distinguish the tow mechanisms and both may be at play. This distinction has been made by some in the sense that if the etiology is due to degeneration of the vein wall, from repeated cannulation trauma, then the abnormality would likely be a pseudoaneurysm while the focal dilatation of the native vein was secondary to increased intraluminal pressure, due to the presence of a distal stenosis, then the abnormality may be an aneurysm [11]. Duplex ultrasound can distinguish aneurysms and pseudoaneurysms.
Fig. 33.5
A right radiocephalic arteriovenous fistula with early aneurysmal degeneration occurring in a bilobed configuration due to repeated needle access in the same location. Access technique needs to be changed to a rope-ladder technique or a buttonhole technique to prevent further aneurysmal degeneration
Current K/DOQI guidelines encourage a “rope-ladder technique” to avoid AVF aneurysmal degeneration unless “buttonhole technique” is being used [12]. The rope-ladder technique is one in which cannulation occurs along the whole length of the vein, thus rotating access sites. The buttonhole technique is that of cannulation in exactly the same location during every dialysis session [13–15].
Elevated mean flow rates. In a large series of AVF aneurysms, mean flow rates were much higher in those without outflow vein stenosis, and these high flow rates are associated with aneurysmal degeneration [5, 6]. High flow was present in 29 % of the cases in one series [7]. The underlying mechanism is thought to be due to abnormal shear stress on the vessel wall, which promotes outward remodeling and gradual dilation with grossly increased caliber of the vessel [16].
History of renal transplantation. Interestingly, multiple patients with AVF aneurysmal degeneration develop diffuse aneurysmal dilation. In one series, 47 % of the patients had a history of renal transplantation. There is speculation that there may be an association between immunosuppression and AVF aneurysm formation [17].
Assessment
In addition to a detailed history about the function of the AVF and any symptoms the patient is experiencing, a thorough physical exam by inspection and palpation is essential in identifying the underlying etiology of the aneurysmal degeneration. A history of prolonged bleeding from the needle access sites and a pulsatile AVF that is hard and non-compressible is suggestive of stenosis in the outflow vein or central venous stenosis (Fig. 33.4). Skin changes such as thinning of the overlying skin may herald future skin necrosis (Fig. 33.6). A history of a herald bleed is especially concerning for impending complete rupture with hemorrhage (Fig. 33.7).
Fig. 33.6
Left brachiobasilic arteriovenous fistula with large aneurysmal degeneration. (a) The aneurysmal degeneration is complicated by skin thinning, depigmentation, and early breakdown (arrow) in addition to chronic arm pain. (b) Circumferentially dissected trilobed aneurysm. One of the aneurysms was treated with excision with end-to-end anastomosis and the remaining two treated with aneurysmectomy and plication. (c) Postoperative week three images
Fig. 33.7
A left brachiocephalic arteriovenous fistula with large multilobed aneurysmal degeneration. The patient presented with acute bleeding and hemorrhagic shock due to necrosis of skin overlying the aneurysmal portion in the upper arm. The aneurysm with overlying eschar through which the patient bled is clearly visible along with old repair sutures at the site of skin breakdown. The fistula was ligated emergently
Objective measurements can be obtained via duplex ultrasound evaluation, a CT angiogram or a diagnostic fistulagram. The duplex ultrasound assesses the diameter of the AVF, areas of stenosis, the presence of laminar thrombus, and flow measurements. As mentioned previously, fistulas with flows greater than 2.0 L/min should be further assessed to determine if intervention is necessary. The presence of hemodynamically significant stenosis or laminar thrombus can lead to technical or mechanical issues with access, which threaten the use of the fistula. Central venous stenosis can be diagnosed or confirmed with a CT angiogram or diagnostic fistulagram. The latter allows concurrent treatment of the stenosis if found.
Management
An aneurysmal AVF may raise concern from the staff, but there is no reason to intervene as long as the AVF is functioning well for dialysis and the dilatation is not steadily and rapidly enlarging [12, 18]. While size alone is not an indication for repair, monitoring for enlargement and symptom development is essential. Current K/DOQI guidelines recommend conservative management of asymptomatic AVF aneurysms by abandoning cannulation in the aneurysmal areas [12]. Using the modified buttonhole cannulation technique has been proposed as a solution for AVF aneurysms [19]. The indications for surgical management include:
The overlying skin condition: Skin thinning or erosion is a marker of impending skin necrosis leading to fistula exposure, subsequent risk for exsanguinating hemorrhage, and subsequent death (Fig. 33.7). In Valenti and colleagues series, type 2 AVF aneurysms had the highest risk of rupture, leading the authors to conclude that these should be carefully monitored for evidence of overlying skin thinning which if present should prompt consideration for prophylactic intervention.
Clinical signs and symptoms:
High-output congestive heart failure (CHF): When a fistula becomes aneurysmal, it can develop flows that are markedly elevated and can result in high-output CHF. Basile and colleagues demonstrated that flows greater than 2.0 L/min are predictive of heart failure, while MacRae and colleagues suggested that the risk of high-flow access on the cardiac function should be entertained when the flow rate is >3000 ml/min [20, 21]. These observations were also confirmed by Pasklinsky and colleagues. In their series of AVF aneurysms, the mean flow in the AVF was 1288 ml/min in those without CHF compared to 2500 ml/min in those with high-output CHF [6].Related posts:
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