Guest:
Dr. Christian de Virgilio is the Chair of the Department of Surgery at Harbor-UCLA Medical Center. He is also Co-Chair of the College of Applied Anatomy and a Professor of Surgery at UCLA's David Geffen School of Medicine.
He completed his undergraduate degree in Biology at Loyola Marymount University and earned his medical degree from UCLA. He then completed his residency in General Surgery at UCLA-Harbor Medical Center followed by a fellowship in Vascular Surgery at the Mayo Clinic.
Resources:
Rutherford Chapters (10th ed.): 174, 175, 177, 178
Prior Holding Pressure episode on AV access creation: https://www.audiblebleeding.com/vsite-hd-access/
The Society for Vascular Surgery: Clinical practice guidelines for the surgical placement and maintenance of arteriovenous hemodialysis access: https://www.jvascsurg.org/article/S0741-5214%2808%2901399-2/fulltext
KDOQI Clinical Practice Guideline for Vascular Access: 2019 Update: https://pubmed.ncbi.nlm.nih.gov/32778223/
Outline:
Steal Syndrome
Definition & Etiology
Steal syndrome is an important complication of AV access creation, since access creation diverts arterial blood flow from the hand.
Steal can be caused by multiple factors—arterial occlusive disease proximal or distal to the AV anastomosis, high flow through the fistula at the expense of distal arterial perfusion, and failure of the distal arterial networks to adapt to this decreased blood flow.
Incidence and Risk Factors
The frequency of steal syndrome is 1.6-9%1,2, depending on the vessels and conduit choice
Steal syndrome is more common with brachial and axillary artery-based accesses and nonautogenous conduits.
Other risk factors for steal syndrome are peripheral vascular disease, coronary artery disease, diabetes, advanced age, female sex, larger outflow conduit, multiple prior permanent access procedures, and prior episodes of steal.3,4
Long-standing insulin-dependent diabetes causes both medial calcinosis and peripheral neuropathy, which limits arteries’ ability to vasodilate and adjust to decreased blood flow.
Patient Presentation, Symptoms, Grading
Steal syndrome is diagnosed clinically.
Symptoms after AVG creation occurs within the first few days, since flow in prosthetic grafts tend to reach a maximum value very early after creation.
Native AVFs take time to mature and flow will slowly increase overtime, leading to more insidious onset of symptoms that can take months or years.
The patient should have a unilateral complaint in the extremity with the AV access. Symptoms of steal syndrome, in order of increasing severity, include nail changes, occasional tingling, extremity coolness, numbness in fingertips and hands, muscle weakness, rest pain, sensory and motor deficits, fingertip ulcerations, and tissue loss.
There could be a weakened radial pulse or weak Doppler signal on the affected side, and these will become stronger after compression of the AV outflow.
Symptoms are graded on a scale specified by Society of Vascular Surgery (SVS) reporting standards:5
Workup
Duplex ultrasound can be used to analyze flow volumes.
A high flow volume (in autogenous accesses greater than 800 mL/min, in nonautogenous accesses greater than 1200 mL/min) signifies an outflow issue. The vein or graft is acting as a pressure sink and stealing blood from the distal artery. A low flow volume signifies an inflow issue, meaning that there is a proximal arterial lesion preventing blood from reaching the distal artery.
Upper extremity angiogram can identify proximal arterial lesions.
Prevention
Create the AV access as distal as possible, in order to preserve arterial inflow to the hand and reduce the anastomosis size and outflow diameter.
SVS guidelines recommend a 4-6mm arteriotomy diameter to balance the need for sufficient access flow with the risk of steal.
If a graft is necessary, tapered prosthetic grafts are sometimes used in patients with steal risk factors, using the smaller end of the graft placed at the arterial anastomosis, although this has not yet been proven to reduce the incidence of steal.
Indications for Treatment
Intervention is recommended in lifestyle-limiting cases of Grade II and all Grade III steal cases.
If left untreated, the natural history of steal syndrome can result in chronic limb ischemia, causing gangrene with loss of digits or limbs.
Treatment Options
Conservative management relies on observation and monitoring, as mild cases of steal syndrome may resolve spontaneously.
Inflow stenosis can be treated with endovascular intervention (angioplasty with or without stent)
Ligation is the simplest surgical treatment, and it results in loss of the AV access. This is preferred in patients with repetitive failed salvage attempts, venous hypertension, and poor prognoses.
Flow limiting procedures can address high volumes through the AV access.
Banding can be performed with surgical cutdown and placement of polypropylene sutures or a Dacron patch around the vein or graft.
The Minimally Invasive Limited Ligation Endoluminal-Assisted Revision (MILLER) technique employs a percutaneous endoluminal balloon inflated at the AVF to ensure consistency in diameter while banding
Plication is when a side-biting running stitch is used to narrow lumen of the vein near the anastomosis.
A downside of flow-limiting procedures is that it is often difficult to determine how much to narrow the AV access, as these procedures carry a risk of outflow thrombosis.
There are also surgical treatments focused on reroute arterial inflow.
The distal revascularization and interval ligation (DRIL) procedure involves creation of a new bypass connecting arterial segments proximal and distal to the AV anastomosis, with ligation of the native artery between the AV anastomosis and the distal anastomosis of the bypass. Reversed saphenous vein with a diameter greater than 3mm is the preferred conduit. Arm vein or prosthetic grafts can be used if needed, but prosthetic material carries higher risk of thrombosis. The new arterial bypass creates a low resistance pathway that increases flow to distal arterial beds, and interval arterial ligation eliminates retrograde flow through the distal artery.
The major risk of this procedure is bypass thrombosis, which results in loss of native arterial flow and hand ischemia. Other drawbacks of DRIL include procedural difficulty with smaller arterial anastomoses, sacrifice of saphenous or arm veins, and decreased fistula flow.
Another possible revision surgery is revision using distal inflow (RUDI). This procedure involves ligation of the fistula at the anastomosis and use of a conduit to connect the outflow vein to a distal artery. The selected distal artery can be the proximal radial or ulnar artery, depending on the preoperative duplex. The more dominant vessel should be spared, allowing for distal arterial beds to have uninterrupted antegrade perfusion. The nondominant vessel is used as distal inflow for the AV access. RUDI increases access length and decreases access diameter, resulting in increased resistance and lower flow volume through the fistula. Unlike DRIL, RUDI preserves native arterial flow.
Thrombosis of the conduit would put the fistula at risk, rather than the native artery.
The last surgical revision procedure for steal is proximalization of arterial inflow (PAI). In this procedure, the vein is ligated distal to the original anastomosis site and flow is re-established through the fistula with a PTFE interposition graft anastomosed end-to-side with the more proximal axillary artery and end-to-end with the distal vein. Similar to RUDI, PAI increases the length and decreases the diameter of the outflow conduit. Since the axillary artery has a larger diameter than the brachial artery, there is a less significant pressure drop across the arterial anastomosis site and less steal. PAI allows for preservation of native artery’s continuity and does not require vein harvest.
Difficulties with PAI arise when deciding the length of the interposition graft to balance AV flow with distal arterial flow.
2. Ischemic Monomelic Neuropathy
Definition
Ischemic monomelic neuropathy (IMN) is a rare but serious form of steal that involves nerve ischemia. Severe sensorimotor dysfunction is experienced immediately after AV access creation.
Etiology
IMN affects blood flow to the nerves, but not the skin or muscles because peripheral nerve fibers are more vulnerable to ischemia.
Incidence and Risk Factors
IMN is very rare; it has an estimated incidence of 0.1-0.5% of AV access creations.6
IMN has only been reported in brachial artery-based accesses, since the brachial artery is the sole arterial inflow for distal arteries feeding all forearm nerves.
IMN is associated with diabetes, peripheral vascular disease, and preexisting peripheral neuropathy that is associated with either of the conditions.
Patient Presentation
Symptoms usually present rapidly, within minutes to hours after AV access creation.
The most common presenting symptom is severe, constant, and deep burning pain of the distal forearm and hand. Patients also report impairment of all sensation, weakness, and hand paralysis.
Diagnosis of IMN can be delayed due to misattribution of symptoms to anesthetic blockade, postoperative pain, preexisting neuropathy, a heavily bandaged arm precluding neurologic examination.
Treatment
Treatment is immediate ligation of the AV access. Delay in treatment will quickly result in permanent sensorimotor loss.
3. Perigraft Seroma
Definition
A perigraft seroma is a sterile fluid collection surrounding a vascular prosthesis and is enclosed within a pseudomembrane.
Etiology and Incidence
Possible etiologies include: transudative movement of fluid through the graft material, serous fluid collection from traumatized connective tissues (especially the from higher adipose tissue content in the upper arm), inhibition of fibroblast growth with associated failure of the tissue to incorporate the graft, graft “wetting” or kinking during initial operation, increased flow rates, decreased hematocrit causing oncotic pressure difference, or allergy to graft material.
Seromas most commonly form at anastomosis sites in the early postoperative period.
Overall seroma incidence rates after AV graft placement range from 1.7–4% and are more common in grafts placed in the upper arm (compared to the forearm) and Dacron grafts (compared to PTFE grafts).7-9
Patient Presentation and Workup
Physical exam can show a subcutaneous raised palpable fluid mass
Seromas can be seen with ultrasound, but it is difficult to differentiate between the types of fluid around the graft (seroma vs. hematoma vs. abscess)
Indications for Treatment
Seromas can lead to wound dehiscence, pressure necrosis and erosion through skin, and loss of available puncture area for hemodialysis
Persistent seromas can also serve as a nidus for infection.
The Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines10 recommend a tailored approach to seroma management, with more aggressive surgical interventions being necessary for persistent, infected-appearing, or late-developing seromas.
Treatment
The majority of early postoperative seromas are self-limited and tend to resolve on their own
Persistent seromas have been treated using a variety of methods-- incision and evacuation of seroma, complete excision and replacement of the entire graft, and primary bypass of the involved graft segment only.
Graft replacement with new material and rerouting through a different tissue plane has a higher reported cure rate and lower rate of infection than aspiration alone.9
4. Infection
Incidence and Etiology
The reported incidence of infection ranges 4-20% in AVG, which is significantly higher than the rate of infection of 0.56-5% in AVF.11
Infection can occur at the time of access creation (earliest presentation), after cannulation for dialysis (later infection), or secondary to another infectious source. Infection can also further complicate a pre-existing access site issue such as infection of a hematoma, thrombosed pseudoaneurysm, or seroma.
Skin flora from frequent dialysis cannulations result in common pathogens being Staphylococcus, Pseudomonas, or polymicrobial species. Staphylococcus and Pseudomonas are highly virulent and likely to cause anastomotic disruption.
Patient Presentation and Workup
Physical exam will reveal warmth, pain, swelling, erythema, induration, drainage, or pus. Occasionally, patients have nonspecific manifestations of fever or leukocytosis.
Ultrasound can be used to screen for and determine the extent of graft involvement by the infection.
Treatments
In AV fistulas:
Localized infection can usually be managed with broad spectrum antibiotics.
If there are bleeding concerns or infection is seen near the anastomosis site, the fistula should be ligated and re-created in a clean field.
In AV grafts:
If infection is localized, partial graft excision is acceptable.
Total graft excision is recommended if the infection is present throughout the entire graft, involves the anastomoses, occludes the access, or contains particularly virulent organisms
Total graft excision may also be indicated if a patient develops recurrent bacteremia with no other infectious source identified.
For graft excision, the venous end of the graft is removed and the vein is oversewn or ligated. If the arterial anastomosis is intact, a small cuff of the graft can be left behind and oversewn. If the arterial anastomosis is involved, the arterial wall must be debrided and ligation, reconstruction with autogenous patch angioplasty, or arterial bypass can be pursued.
References
1. Morsy AH, Kulbaski M, Chen C, Isiklar H, Lumsden AB. Incidence and Characteristics of Patients with Hand Ischemia after a Hemodialysis Access Procedure. J Surg Res. 1998;74(1):8-10. doi:10.1006/jsre.1997.5206
2. Ballard JL, Bunt TJ, Malone JM. Major complications of angioaccess surgery. Am J Surg. 1992;164(3):229-232. doi:10.1016/S0002-9610(05)81076-1
3. Valentine RJ, Bouch CW, Scott DJ, et al. Do preoperative finger pressures predict early arterial steal in hemodialysis access patients? A prospective analysis. J Vasc Surg. 2002;36(2):351-356. doi:10.1067/mva.2002.125848
4. Malik J, Tuka V, Kasalova Z, et al. Understanding the Dialysis access Steal Syndrome. A Review of the Etiologies, Diagnosis, Prevention and Treatment Strategies. J Vasc Access. 2008;9(3):155-166. doi:10.1177/112972980800900301
5. Sidawy AN, Gray R, Besarab A, et al. Recommended standards for reports dealing with arteriovenous hemodialysis accesses. J Vasc Surg. 2002;35(3):603-610. doi:10.1067/mva.2002.122025
6. Thermann F, Kornhuber M. Ischemic Monomelic Neuropathy: A Rare but Important Complication after Hemodialysis Access Placement - a Review. J Vasc Access. 2011;12(2):113-119. doi:10.5301/JVA.2011.6365
7. Dauria DM, Dyk P, Garvin P. Incidence and Management of Seroma after Arteriovenous Graft Placement. J Am Coll Surg. 2006;203(4):506-511. doi:10.1016/j.jamcollsurg.2006.06.002
8. Gargiulo NJ, Veith FJ, Scher LA, Lipsitz EC, Suggs WD, Benros RM. Experience with covered stents for the management of hemodialysis polytetrafluoroethylene graft seromas. J Vasc Surg. 2008;48(1):216-217. doi:10.1016/j.jvs.2008.01.046
9. Blumenberg RM, Gelfand ML, Dale WA. Perigraft seromas complicating arterial grafts. Surgery. 1985;97(2):194-204.
10. Lok CE, Huber TS, Lee T, et al. KDOQI Clinical Practice Guideline for Vascular Access: 2019 Update. Am J Kidney Dis. 2020;75(4):S1-S164. doi:10.1053/j.ajkd.2019.12.001
11. Padberg FT, Calligaro KD, Sidawy AN. Complications of arteriovenous hemodialysis access: Recognition and management. J Vasc Surg. 2008;48(5):S55-S80. doi:10.1016/j.jvs.2008.08.067
