A master class was held at the Vascular Access at Charing Cross (VA@CX2017) conference in April 2017 with invited experts and active audience participation to discuss arteriovenous (AV) vascular access aneurysms, a serious and common complication of vascular access (VA). The natural history of aneurysms in VA is poorly defined, and although classifications exist they are not uniformly applied in studies or clinical practice. True and pseudo aneurysms of AV access occur. Whilst an AV fistula by definition is an abnormal dilatation of a blood vessel, an agreed definition of 18 mm, or 3 times accepted maturation diameter, is proposed. The mechanism of aneurysmal dilatation is unknown but appears to be a combination of excessive external remodeling, wall changes due to injury, and obstruction of outflow. Diagnosis of AV aneurysms is based on physical examination and ultrasound. Venography and cross-sectional imaging may assist and be required for the investigation of outflow stenosis. Treatment of pseudo aneurysms and true aneurysms of VA (AVA) is not evidence-based, but relies on clinical experience and available facilities. In many AVA, a conservative approach with surveillance is suitable, although intervals and modalities are unclear. Avoidance of rupture is imperative and preemptive treatment should aim for access preservation, ideally with avoidance of prosthetic materials. Different techniques of aneurysmorrhaphy are described with good results in published series. Although endovascular approaches and stenting are described with good short-term results, issues with cannulation of stented areas occur and, while possible, this is not recommended, and long-term access revision is recommended.
J Vasc Access 2017; 18(6): 464 - 472
Article Type: REVIEW
AuthorsNicholas Inston, Hiren Mistry, James Gilbert, David Kingsmore, Zahid Raza, Matteo Tozzi, Ali Azizzadeh, Robert Jones, Colin Deane, Jason Wilkins, Ingemar Davidson, John Ross, Paul Gibbs, Dean Huang, Domenico Valenti
- • Accepted on 12/10/2017
- • Available online on 02/11/2017
- • Published in print on 17/11/2017
This article is available as full text PDF.
Following the creation of vascular access, aneurysm formation is common and can result in serious and devastating complications. The natural history of aneurysms of vascular access (AVA) is largely unknown, partly due to the lack of application of standardized terminology. Perhaps more perplexingly, many guidelines do not use classification to guide treatment. This may reflect the differing classifications that are available, based on clinical morphology or imaging appearances. The aims of the Charing Cross Masterclass was to explore the subject in depth and to bring together published evidence, expert opinion, and experience to produce this detailed state of the art review with recommendations and consensus statements following from discussion and further analysis of the published data.
Pathophysiology and mechanisms
If defined as an abnormal dilatation of a blood vessel then it can be argued that all mature arteriovenous fistulas (AVF) are aneurysms. Obviously, this definition is not clinically helpful and a more detailed classification is required. What is more relevant is the distinction between controlled dilatation and maturation in a fistula and uncontrolled expansion either locally or throughout the AVF.
It is often proposed that aneurysms are the result of repeated cannulation leading to multiple small fibrous scars in the vessel wall, which expand with time due to a lack of elasticity within the scar tissue. Whilst this is a contributing factor in many AVA, the areas where needling has not been performed can be aneurysmal and can occur in patients who remain predialysis, never having needled the AVFs.
The most widely accepted mechanism of AVF maturation and dilatation is the effect of wall shear stress (WSS), which causes reactive changes in the vessel wall. When an anastomosis is formed and arterial flow enters the lower resistance venous system, novel forces are experienced by the venous endothelium. The radial forces increase and the transmural wall pressure increases. This is modest, and has been shown to be similar at 1 week and 6 weeks following AVF formation (1). The main driver of vessel remodeling is WSS, which increases rapidly following clamp release. Sustained increases in WSS results in the activation of enzymes via endothelial cell signaling, particularly matrix metalloproteases, which allow structural changes within the vein wall and result in dilatation and remodeling (2, 3). As the vessel diameter increases, the WSS decreases, which results in negative feedback. It can be calculated that doubling the vessel diameter results in a tenfold decrease in WSS, thus limiting subsequent further dilatation. Flow within an AVF is not uniform and WSS is not constant. Turbulence and spatial and temporal gradients occur (4), which may stimulate the vessel wall to remodel further. If the vessel wall is prone to dilatation, this process may become exaggerated.
Although conditions, such as connective tissue disorders (5), Alport’s disease (6), adult polycystic kidney disease (7), and pregnancy (8) have been proposed as risk factors for AVA, the precise pathophysiological mechanism remains unclear. Histological examination of resected fistula aneurysms reveals infiltration of collagen with thickening and altered architecture of the vessel wall (8). These observations may support irregular or defective collagen deposition as a further risk in AVA pathogenesis.
The role of stenoses in aneurysm formation is the result of an exacerbation of abnormal hemodynamics as well as increased pressure. Downstream of a stenosis, due to the Bernoulli effect, marked defragmentation in WSS occurs. If outflow, or central stenoses are present in an AVF, increased transmural pressure occurs, thus promoting wall distension. This is particularly true in areas that are already aneurysmal (9).
Aneurysms in arteriovenous (AV) access are due to a combination of hemodynamic responses with or without existing or genetically predetermined wall abnormalities resulting in excessive dilatation, which may be worsened by increased pressure due to an outflow stenosis. They cannot be accurately predicted in any patient group, although some disease states may be higher risk.
Terminology, definitions, and classification
AVA generally can be regarded as abnormal dilatation of blood vessels but they are heterogeneous in their morphology and represent a diverse range of presentations. Agreement and standardization of the definitions and classification of AVA are required to improve professional communication and documentation, to aid the study of the natural history, and to improve management modalities and the best timing of intervention.
The distinction between pseudoaneurysms (pAVA) and true aneurysms (AVA) is clearly defined. pAVA represent a hematoma that is in direct communication with the vessel lumen, which develop a fibrotic “sac” but this is devoid of endothelium or a recognizable vascular wall structure, hence the term “false aneurysm.” Size does not define pAVA, and many small ones may go clinically undetected.
In contrast, “true” aneurysms are a dilatation of the vessel itself and have a wall that is composed of all layers of a vascular structure. As all fistulas are distended vessels size is used as a basis of define them. In clinical practice, size has been the main defining parameter used. Studies have defined an absolute size. Using 3 times the normally defined mature size of 6 mm, Valenti et al (15) suggests >18 mm as a defining diameter. This was also used by Balaz and Björck (16). Others have used size alone (>40 mm) (17) or comparative diameter size compared to the rest of the access; 2 times greater than rest of the access (18); and 3 times larger than other segments in the AVF suggested (19, 20). A combination of comparative and absolute size has also been suggested (3 times larger than an autologous vessel or more than 20 mm) (8). Vesely (21) suggested defining AVA only when increased intraluminal pressure occurs due to outflow stenosis, although defining this clinically may be difficult.
It would appear that most definitions include an expansion of threefold, and an absolute of around 18 mm, which would appear to be a reasonable working definition.
Further subclassification of AVA based on morphology has been attempted (see
Classifications of aneurysms in AVF
|AVF = arteriovenous fistulas.|
|Valenti et al (15)(>18 mm)||Type 1||Dilatation of the whole (1a) or proximal aspect (b) of the AVF|
|Type 2||“Camel hump” appearance with two distinct aneurysms|
|Type 3||Complex aneurysms|
|Balaz and Björck (16)(>18 mm)||Type 1||Without stenosis|
|Type 2||Significant stenosis (>50%)|
|Type 3||Partial thrombosis (<50% lumen)|
|Type 4||Complete thrombosis|
Valenti et al (15) described 4 subtypes of AVA based on external appearance. Type 1 is a dilatation of the whole (1a) or the proximal aspect of the AVF (1b); Type 2 has a camel hump appearance with >1 discrete aneurysms; Type 3 is a complex and heterogeneous AVA; and Type 4 is pAVA.
Balaz and Björck (16) suggested a slightly different classification based on the presence of stenosis or thrombosis identified with ultrasound or fistulogram. They describe Type 1 as being without stenosis; Type 2 with significant stenosis (>50%); Type 3 with partial thrombosis (>50% lumen); and Type 4 with complete thrombosis.
The primary purpose for the classification of AVA in practice is to allow the standardization of terminology to permit accurate communication and standardize the studies. The standard definition of an AVA is based on 3 times the accepted maturation diameter (3 × 6 mm), and 18 mm is proposed. Morphological classification based on clinical findings can be used by multiple healthcare settings and can be applied without investigations. More detailed classification based on imaging may be useful, particularly within studies.
Incidence and natural history
Huber et al (22) reported the incidence to be 4% in a large series of access, both grafts and fistulas, but other series have reported the incidence as being between 5% and over 60% (8, 15, 23-24-25). This variation is likely to represent issues with defining AVA rather than true variation, as well as prevalent versus incident reporting. The anatomical site of the AVF has shown differences with proximal fistulas having a higher rate than distal fistulas, and the cephalic vein is affected rather than the basilic vein (8).
Longitudinal studies of the natural history of AVA are few. Patients who were classified according to the Valenti classification were followed up for 2 years. Of those with AVFs, 13.5% of low clearance patients had AVA, whereas those on dialysis had a much higher incidence (43.5%). The age of the aneurysmal fistula was between 521 days and 2,521 days. This is consistent with other studies of AVA where the average age of the AVF was between 16.5 and 72.8 months when treatment was initiated (range 12-136 months) (8, 26-27-28-29-30-31).
In most cases, AVA remain stable and asymptomatic without jeopardizing the functioning of the access or the hemodialysis. This was particularly true for type 1a and 1b AVA where complications were low. The main risks of AVA, those of bleeding, were seen in Type 2a and 2b fistulas (15).
Studies on the prediction of the rate of expansion, skin changes, and an increase in flow rates have not been performed.
pAVA are commonly seen on routine venograms, and small pAVA are innocuous and represent cannulation points. However, the natural history of larger pseudo-aneurysms is to expand and result in catastrophic rupture. In polytetrafluoroethylene (PTFE) grafts, the prevalence of pAVA is estimated at between 2% and 50% (32, 33).
pAVA at the level of the anastomosis often occurs early postoperatively due to surgical bleeding or possibly anastomotic infection. The cannulation of an AVF or arteriovenous graft (AVG) during dialysis, or from intervention, can also result in pAVA formation (33).
Most data are from traditional PTFE (tAVG) rather than “early-cannulation” (ecAVG), or biologic (bAVG). Primary aneurysmal degeneration of tAVG is possible, similar to the dilatation of vascular bypass grafts seen over many years, although patient mortality may precede this. More commonly, pAVA secondary to cannulation are seen in tAVG. A recent review reported an incidence of up to 40% in tAVG and cites pAVA as the leading cause of graft loss after 2 years (34).
The natural history of AVG pAVA is typically from multiple areas of adjacent punctures, which coalesce and form larger broader-based pAVA with a high risk of expansion and bleeding. Inexperienced cannulation and movement can result in tears in the graft or more commonly puncture the back wall of the AVG where pressure cannot be easily applied.
The introduction of grafts with “self-sealing” properties allowing ecAVG may reduce early pAVA and 3 reviews on the safety and efficacy of reported complications relating to surgical anastomosis rather than cannulation, although data are based on small case series with short follow-up, and pAVA has been described after 2 years in ecAVG (35-36-37).
Data from biological grafts are sparse, but may historically represent manufacturing issues. Modern biological grafts do not appear to have a high rate of aneurysm formation (38).
Due to lack of agreed definitions, the incidence of pAVA and AVA is unknown. When the prevalence is assessed in dialysis populations using a definition of 18 mm it appears to be common (>40%) although those requiring treatment are less (approx. 5%). The natural history of AVA is poorly understood although those patients requiring treatment in studies had long-standing AVA suggesting a late and/or progressive process.
Ultrasound provides a useful noninvasive, noncontrast medium modality for assessment and surveillance of both pAVA and true AVA. In pAVA, the size of the aneurysm sac and the width of the neck should be assessed, as should flow and thrombus within the sac. Inflow and outflow vessels and wall characteristics, such as thickness and infection, also may be possible to assess with Ultrasound scan (USS) (39, 40).
Likewise, in AVA, sonographic assessment should include transverse and longitudinal measurements at defined points, and the assessment of flow and thrombus.
Proximal and distal stenoses should be identified, although formal radiological (41) assessment may be required. Diagnostic venography in isolation is almost obsolete and is reserved for cases where intervention is planned or anticipated, or in circumstances where ultrasound is inconclusive or less helpful, such as in the assessment of the central thoracic veins. Computed tomography (CT) incurs much higher doses of ionizing radiation and magnetic resonance imaging (MRI), although highly sensitive and specific for stenosis detection, may be limited in availability, and is time consuming.
Venography should be reserved for assessing the symptomatic or rapidly expanding aneurysmal AV access where a downstream stenosis is suspected and where angioplasty and/or stenting is anticipated. Venography provides a roadmap of the access outflow through to the right atrium, and allows dynamic assessment as the image is acquired. Its main drawback is its 2-dimensional (2D) nature, and occasionally orthogonal views (i.e., venograms taken in more than 1 angular projection) are required for accurate diagnosis and subsequent treatment of a symptomatic stenosis. Intravascular ultrasound can be a helpful adjunct to venography in this scenario.
The Balaz and Björck (16) classification relies on a description of stenosis and thrombosis, and diagnostic venography may be required. As the reported incidence of stenosis in aneurysmal AV access outflow is from 13% to 100%, venography should be considered in nonemergent cases and where surgery is anticipated (5, 20, 42, 43).
In patients allergic to iodinated contrast or who are in the predialysis window, carbon dioxide venography can be useful and has been shown to have a high degree of accuracy in stenosis detection comparable with iodinated contrast (44).
CT and MRI provide high-resolution 3D imaging of access from the inflow artery to the right atrium, and high rates of specificity, sensitivity, and accuracy in detecting stenosis have been reported with the use of CT (46). Due to its radiation dose, CT should be reserved for more problematic cases. MRI can provide even further soft tissue definition, but is rarely used in access.
The investigation and surveillance of pAVA and AVA is generally USS-based along with clinical examination to guide further imaging. Venography is indicated where outflow stenosis is suspected and intervention anticipated, or prior to surgical intervention if it is nonemergent as outflow stenosis is common in symptomatic AVA. Cross-sectional imaging with CT or MRI may be useful in some patients.
A small number of AVA will present as a life-threatening hemorrhage from a free rupture. However, a ruptured fistula should represent a failure of care, both in recognizing the early signs of potential imminent rupture and in treating complications that ultimately lead to rupture.
The predictors of rupture are similar for pAVA and AVA. Pain and/or rapid expansion, thin shiny or necrotic skin overlying the AVA, scabs, ulceration, or signs of infection are all harbingers of imminent rupture and mandate urgent intervention.
Treatment of a ruptured pAVA or AVA, where flows can be high (liters/minute) requires emergency measures. Often a “herald” bleed may be the first sign and this should not be underestimated. The incidence of VA hemorrhage is unknown and may represent a significant cause of mortality in the dialysis population. Resuscitative measures with control of bleeding is required. Definitive treatment for life-threatening bleeding from an AVA is ligation, although fistula salvage (47) may be achieved if bleeding is adequately controlled. Blood loss from inflow and outflow can be dramatic. In anastomotic pAVA, and especially in infection, arterial reconstruction may be required.
One area of diagnostic confusion is the fistula “blow” when a perifistula hematoma forms as a result of a leak around a dialysis needle, needle dislodgement at the time of dialysis, or failure to achieve adequate hemostasis after the removal of a dialysis needle. These hematomas can be both large and painful, but are almost universally self-limiting and best treated conservatively.
In less emergent situations, the indications for surgery are ill defined but relate to either the clinical effects of the aneurysm and/or the prevention of rupture and bleeding. Clinical effects may be related to high flow and cardiovascular risks, or may be patient related, including discomfort or aesthetics. Intervention for cosmetic reasons alone are controversial, but if access-preserving reduction treatments improve quality of life and avoid future line use, then they should be carefully considered. Conservative treatment should include the investigation of outflow stenosis and modification of the cannulation sites and the technique (48).
Clinical indications of significant outflow stenosis include a tense AVF, which does not collapse on occlusion and elevation, minimal or no-pulse augmentation, prolonged bleeding time, and high venous pressure on dialysis (49).
The risk of rupture is associated with an increasing rate of growth, and >10% increase in diameter per year has been cited as a risk in other aneurysms (28, 50), although this is likely an overestimate for AVAs (51). At this rate of expansion, many true AVA will be simply monitored more frequently, although the data to determine the timing of surveillance intervals are not defined.
If symptoms and signs indicate that treatment is required, then ligation of the access at the origin is a simple and effective technique. Unfortunately, the access is lost and the aneurysmal sac may become thrombosed, resulting in thrombophlebitis and a cosmetically unacceptable result (8). In addition, aneurysms of the stump and the artery have been described (52, 53).
The desired outcome of intervention should be the preservation of definitive dialysis access, and surgical options to salvage the access should be the first choice.
The choice of technique for access-preserving surgery is predominately based on the morphology of the aneurysm. In small and discrete AVA in a tortuous AVF, it often possible to excise, mobilize, and reconstruct the AVF directly (30). If skin is compromised a “trap door” flap technique can be used (30, 54).
In any AVA with skin compromise, infection should be assumed, and systemic and topical antibiotics used particularly when prosthetic material is used.
As fistula ligation may result in phlebitis in the remnant, this may mimic graft infection, particularly if the graft is in an adjacent position. In addition, unless it is marked, cannulation may be difficult in the new graft. It is recommended that should an AVG be required, an early cannulation graft is used to avoid central venous catheter (CVC) use.
To preserve the access, and avoid prosthetic materials, techniques of reduction aneurysmorrhaphy have been described. The method of reduction involves plication and excision of the remaining redundant tissue, and this can be guided by a Foley catheter or surgical dilator to ensure that adequate luminal diameter is retained (26, 27, 57-58-59-60).
Suture plication may be used, but techniques using surgical stapling devices which were first described by Hakim in 1997 (61) and modified by other authors (8, 2862, 63) The advantages being a quicker operative time and the ability to cannulate immediately thus avoiding central venous catheters (29).
The use of a reinforcing external prosthesis has been described following aneurysmorrhaphy. Balaz et al (64) described the technique in a small series, although long-term data were not presented. Berard et al (20) also reported the use of a polyester external reinforcing prosthesis in 33 patients; however, 49% were performed for flow reduction rather than purely for aneurysm treatment. While neither study showed significant rates of infection, the technique introduces prosthetic material, whereas other techniques have shown comparable outcomes with aneurysmorrhaphy alone (see
Summary of studies of surgical revision of aneurysms in autogenous vascular access (excluding prosthetic grafts and pseudo aneurysms)
|Study||Technique||Study type (n = patients)||Outcome|
|AVF = arteriovenous fistulas; ECM = extracellular matrix; FU = follow up.|
|Vo et al (28)||Stapled aneurysmorrhaphy||Observational series (n = 40)||Primary assisted patency 88% at 1 year|
|Hossny (27)||Partial aneurysmectomy, with or without reduction venoplasty||Observational series (n = 14)||Patency at 1 year was 85.7%|
|Berard et al (20)||Externally reinforced aneurysmorrhaphy||Observational series (n = 38)||Primary 1 year patency was 93%|
|Piccolo et al (63)||Stapled aneurysmorrhaphy||Observational series (n = 13)||Primary assisted patency of 90% (6 months)|
|Furukawa (59)||Surgical revision, surgical plication||Observational series (n = 23)||n/a|
|Tozzi et al (29)||Stapled aneurysmorrhaphy||Observational series (n = 14)||Primary functional patency 85.7%|
|Woo et al (26)||Reduction-resection technique||Observational series (n = 19)||Median primary patency = 14 mo|
|Sigala et al (31)||Autologous reconstruction||Observational series (n = 31)||Primary patency at 1 year = 87%|
|Georgiadis et al (51)||Resection or partial resection||Observational series (n = 26)||Primary patency at 1 year = 69%|
|Pasklinsky et al (8)||Ligation; Excision and autologous or prosthetic interposition||Observational series (n = 23)||n/a|
|Rokošný et al (19)||Reinforced aneurysmorrhaphy||Observational series (n = 62)||Primary assisted patency at 12 months = 80%|
|Moreira et al (65)||Excision, reduction and reimplantation||Case report (n = 1)||n/a|
|Belli et al (55)||Excision and primary repair or interposition graft||Observational (n = 26)||Primary patency (noninterventional) at 12 months = 52%|
|Almehmi and Wang (30)||Partial aneurysmectomy||Observational series (n= 36)||Assisted primary patency at 6 months (97%)|
|Uysal and Ceviker (58)||Sutured aneurysmorrhaphy||Case report (n = 1)||Patent at 6 months|
|Al-Thani et al (56)||Ligation; excision and repair with graft interposition or vein interposition; end-to-end AVF||Observational study (n = 36)||n/a|
|Patel et al (43)||Aneurysmorrhaphy (single and two stage)||Observational study (n = 48)||Patency 100% (<1 year of FU)|
|Baker and Malgor (57)||Stapled aneurysmorrhaphy||Case report (n = 1)||Patent at 1 year|
|DuBose et al (66)||Interposition Tubularized CorMatrix(®) ECM graft||Observational series (n = 15)||86.6% patency at 6.9 months|
|Powell et al (67)||Long segment plication||Observational series (n = 35)||n/a|
|Wang and Wang (68)||Partial aneurysmectomy and repair (PAR)||Observational series (n = 185)||Primary assisted patency 1 year = 96%|
|Balaz et al (64)||Aneurysmorrhaphy, with external polyethylene terephthalate (PET) prosthesis||Case series (n = 4)||n/a|
|Karabay et al (69)||Resection of the aneurysm||Observational series (n = 18)||n/a|
|Pierce et al (62)||Stapled Reduction aneurysmoplasty||Observational series (n = 12)||n/a|
Unfortunately, due to different reported outcome measures, the reported results of surgical treatment of AVA are variable; however, in many studies, patency at 1 year of between 52% and 100% (shown in
Endovascular techniques alone have been used to treat VA aneurysms in a small number of series (see
Endovascular interventions of aneurysms and pseudo aneurysms
|Reference||Technique||Outflow stenosis||Study type (n = patients)||Outcome|
|PTFE = polytetrafluoroethylene; AVG = arteriovenous graft; AVF = arteriovenous fistulas.|
|Shemesh et al (42)||Endovascular stent graft exclusion with outflow/central vein plasty||100%||Observational series (n = 20)||87% at 12 months|
|Shah et al (70)||Stent graft exclusion (Pseudoaneurysms) ± central venoplasty||56%||Observational series (n = 24)||Patency at 180 days = 69.2%|
|Zink et al (18)||Endovascular stent graft exclusion with outflow/central vein plasty||76.3%||Observational series (n = 38)||Assisted patency at 180 days = 76.3%|
|Pandolfe et al (71)||Stent grafts in HD AV grafts||n/a||Case series (n = 4)||Patency = 75% at 3 months|
|Fotiadis et al (72)||Stent grafts exclusion of symptomatic hemodialysis graft pseudoaneurysms||63.6%||Observational series (n = 11)||Access patency (secondary) 72.7% at 6 months|
|Barshes et al (73)||Self-expanding stent grafts||n/a||Observational series (n = 26)||28% primary patency and 6 months|
|Vesely (74)||Stent graft to repair a in PTFE hemodialysis graft||n/a||Observational series (n = 11)||20% primary patency at 6 months|
|Najibi et al (75)||Covered stent (Wallgraft) for exclusion of AVG and AVF pseudoaneurysms.||n/a||Observational series (n = 10)||70% patency at 6 months|
|Ryan et al (76)||Covered stent (Wallgraft) for pseudoaneurysms of AVG and AVF||n/a||Case series (n = 4)||100% patency and 3 months|
|Mantha et al (77)||PTFE covered stents to exclude aneurysms||n/a||Case report||n/a|
As aneurysms are more common at cannulation sites, the use of stent grafts to preserve access may result in inadvertent needling or necessitate cannulation through the stent wall despite cannulation being contraindicated in all cases.
Problems associated with stent graft needling include, but are not limited to, the technical aspects of cannulation, infection, further pseudoaneurysm formation, stent fracture, or disintegration. In a retrospective review of stent grafts placed for aneurysms and pseudo aneurysms in vascular access, a 28.9% complication rate related to stent migration, fracture, erosion, or rupture was noted (18). A further study showed that stent grafts used in hemodialysis had a higher rate of infection (42.1% vs. 18.2%) than in other pAVA treated this way (78, 79).
Patients should be counselled and consent to these risks, and where stent graft cannulation is unavoidable it should ideally be “prescribed,” so there is no doubt among the nursing team about the intended plan for the access. Smaller gauge needles are recommended and buttonhole cannulation is avoided to prevent disruption of the stent graft skeleton. Ultrasound may be required to locate the lumen and to assist needling, as well as to monitor pseudoaneurysm formation and stent disruption (71, 80).
The treatment of pAVA and AVA is guided by clinical experience rather than evidence. In many AVA, a conservative approach with surveillance is sufficient. Ruptured AVA present with symptoms and signs prior to rupture, and education programs should be directed to recognize these.
Surgical approaches remain the mainstay of treatment, although endovascular stenting has shown good results and may be useful in frail patients. Multiple techniques of access preservation with the avoidance of prosthetic materials is described with good results, and should be considered where possible. Stent cannulation is possible but not recommended.
Abnormal hemodynamics in AV access may result in excessive remodeling of vessels and the occurrence of arteriovenous aneurysms. They are a relatively common finding in vascular access, and the incidence is variable due to definitions that are not standardized. There is a requirement for more consistent definitions to better understand both the natural history and the best management options.
The avoidance of complications of pAVA and AVA is essential as rupture is a life-threatening emergency, and all members of the VA team – including the patient – should be educated to identify early signs of potential rupture.
Studies to define the natural history of different aneurysm types, their growth rates, and the timing of intervention are required. The best treatment modality is not clear, and different techniques have been described. However, those techniques that preserve access patency and avoid prosthetic materials appear to be safe and have excellent results.
- Inston, Nicholas [PubMed] [Google Scholar] 1, * Corresponding Author (email@example.com)
- Mistry, Hiren [PubMed] [Google Scholar] 2
- Gilbert, James [PubMed] [Google Scholar] 3
- Kingsmore, David [PubMed] [Google Scholar] 4
- Raza, Zahid [PubMed] [Google Scholar] 5
- Tozzi, Matteo [PubMed] [Google Scholar] 6
- Azizzadeh, Ali [PubMed] [Google Scholar] 7
- Jones, Robert [PubMed] [Google Scholar] 1
- Deane, Colin [PubMed] [Google Scholar] 2
- Wilkins, Jason [PubMed] [Google Scholar] 2
- Davidson, Ingemar [PubMed] [Google Scholar] 8
- Ross, John [PubMed] [Google Scholar] 9
- Gibbs, Paul [PubMed] [Google Scholar] 10
- Huang, Dean [PubMed] [Google Scholar] 2
- Valenti, Domenico [PubMed] [Google Scholar] 2
Department of Renal Surgery and Vascular Access, Queen Elizabeth Hospital, University Hospital Birmingham NHS Foundation Trust, Birmingham - UK
Department of Vascular Surgery, King’s College Hospital, Denmark Hill, London - UK
Oxford Transplant Centre, Churchill Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford - UK
Department of Vascular Surgery and Renal Surgery, Queen Elizabeth University Hospital, Glasgow - UK
Vascular Surgical Service, Royal Infirmary of Edinburgh, Edinburgh - UK
Vascular Surgery, Department of Surgery and Center for Research on Organ Transplantation, Insubria University School of Medicine, Circolo University Hospital, Varese - Italy
Department of Cardiothoracic and Vascular Surgery, McGovern Medical School at The University of Texas Health Science Center at Houston, Houston, Texas - USA
Department of Surgery, Tulane University, New Orleans, Louisiana - USA
Dialysis Access Institute, Orangeburg Regional Medical Center, Orangeburg, South Carolina - USA
Wessex Kidney Centre, Queen Alexandra Hospital, Portsmouth - UK