The arteriovenous (AV) fistula is regarded as the vascular access of choice for hemodialysis (HD) because of its superior patency and low complication rates. Even so, this type of vascular access can result in severe complications, among them, thrombosis of the shunt. This complication usually results from stenotic lesions in the venous outflow system. Inflow arterial obstruction is not an uncommon complication of the AV fistulas, but also most often starts in the venous system and extends into the juxta-anastomotic artery. A true inflow stenosis results from an embolus, originating from the proximal arterial system, a so-called arterial-to-arterial embolization. Although such stenosis occurs infrequently, it can lead to acute inflow obstruction and cause sudden fistula failure and limb-threatening acute ischemia.
A 63-year-old Hispanic patient with end stage renal disease (ESRD) developed sudden failure of his right forearm AV fistula in the middle of a dialysis session. On further questioning, he complained of numbness and weakness in the right hand. Physical examination revealed evidence of a nonfunctioning dialysis fistula, as well as findings suggestive of acute hand ischemia. His past history was significant for hypertension and diabetes mellitus. An immediate Doppler examination revealed no signals in the vessels distal to the fistula. A clinical diagnosis of AV fistula failure with acute hand ischemia was made, and emergency exploration of the right brachial artery was performed. A 3 cm transverse incision was made over the distal arm, and the brachial artery was exposed proximal to the fistula and isolated. A brachial arteriotomy and angiogram were performed, demonstrating an embolus, which occluded the arterial inflow tract of the fistula. An emergency embolectomy and thrombolysis restored the patency of the fistula and the hand vascularity. Intravenous heparin anticoagulation was started postoperatively. Eight hours after the surgery, he developed bleeding from the wound site and hematoma over the incision site. An operative reexploration was undertaken, hemostasis was achieved, hematoma evacuated, and heparin was discontinued. The fistula patency and the hand vascularity remained normal in the postoperative period. The intravenous heparin was restarted 24 hours later. In the subsequent work up, an echocardiogram and CT imaging revealed the presence of extensive atherosclerosis of the aorta and type B dissection. The evaluation of the heart did not reveal any source for the embolus. The atherosclerotic thrombus in the aortic arch was considered to be the source of the embolus. He recovered well from the procedure, and the hemodialysis was restored through the fistula. He was discharged home on oral anticoagulation.
Radio-cephalic arteriovenous fistulas using native vessels are the first choice for vascular access in the dialysis of ESRD patients, but are associated with dysfunction and complications.1 Thrombosis of the fistula is the most common cause of fistula failure.3,4 The most important predisposing factor for thromboses is venous stenosis, which accounts for 80–85% of complications; it is initiated by local endothelial cell injury to the vessels.6,7 Uncorrectable thrombosis in fistulas account for 80–85% of AV fistulas loss.7 Other complications include aneurysm formation, steal syndrome, venous hypertension, hemorrhage, infections, and even congestive heart failure and neurological disorders.2 African American females, diabetics, and elderly patients appear to be at increased risk for complications associated with their vascular access for dialysis.2 Another cause of AV fistula complication is stenosis of the artery feeding the shunt. This complication can be related to problems on the venous system side of fistulas, from which thrombi can extend to 1 to 2 cm into the juxta-anastomotic artery.7 This is the main reason why the inflow stenosis is common, having an incidence from 14–42%.9 Non-anatomic problems relating to occlusion of the artery include hypotension, high hematocrit levels, hypovolemia, hypercoagulable states, and excessive post-dialysis fistula compression.6,8 All of these complications lead to the fact that the cumulative AV fistula patency in most centers ranges from 60–70% at 1 year and 50–60% at 2 years.5 True inflow stenosis occurring from an embolus from the proximal arterial system is a more serious condition. An acute inflow arterial stenosis causing sudden fistula failure from a thromboembolism has never before been reported. In the case reported here, the inflow embolism and subsequent stenosis reduced the luminal diameter of the normal feeding artery by more than 50%, jeopardizing the vascularity of the limb and the fistula patency. In such cases, immediate aggressive evaluation of the above vascular system is necessary to try to prevent other similar episodes. The heart is by far the predominant source of arterial thromboembolisms, being the site of origin in 80–90% of cases in all reported series.10 Atheromas of the aorta as a source of peripheral embolism, as happened in our case, is a rare but well-recognized entity. The advent of transesophageal echocardiography and magnetic resonance imaging, as well as more frequent use of computed tomography scans have led to the identification of the aorta as the source of peripheral emboli.11 In a prospective study of 89 patients with embolic events, Reber et al12 found that aortic thrombi were sources of emboli in 9% of patients. The risk of thromboembolism or atheroembolism in patients with aortic atherosclerosis is markedly increased when transesophageal echocardiography reveals protruding plaques thicker than 4 mm.13,14 In the event of a peripheral embolic episode, as happened in our patient, a prompt surgical intervention and embolectomy should be undertaken to restore the vascularity of the affected part. There is no consensus regarding the best therapeutic approach to deal with atheromas in the aorta. Surgery has been advocated as a definitive treatment,12,15 but anticoagulation has been used successfully, thereby avoiding the morbidity and mortality associated with major aortic surgery.16 Our patient was treated successfully with anticoagulation. In summary, this case highlights the possibility of inflow embolism as a cause of fistula failure and underscores the importance of careful vascular examination in all such patients.
All patients who present with nonfunctioning AV fistula and acute hand ischemia should be carefully evaluated to determine the possibility of an unusual cause of fistula failure.
How Would You Treat This Patient?
Lawrence Garcia, MD
Caregroup/Harvard Medical School,
Acute arterial occlusions invariably are medical emergencies. These include acute myocardial infarctions (STEMI), embolic mesenteric ischemia, or, as in this case report, acute limb ischemia. The case report by Kumaran et al describes an acute arterial occlusion at the site of an arterial-venous (AV) fistulae.
A 63-year-old male developed sudden failure of his AV fistulae. A prompt physical examination revealed a non-functioning dialysis fistulae and diagnosis of an acute emboli. The therapy embarked upon by the authors was an open, emergent embolectomy and re-establishing flow to the distal vessels and hand, with salvage of the fistulae. Atherosclerosis from the aorta was considered to be the ultimate cause of the embolus. Although the patient also had an evident type B aortic dissection, this was not considered the primary cause for the embolus.
An open surgical embolectomy remains the “gold” standard for initial therapy in this patient. An alternative to this surgical approach would be an endovascular approach. Although the patient in the case report recovered fully and had no surgical complications, an open surgical approach may still have potential complications, such as hematoma, bleeding, infection, and myocardial infarction. The benefits of an endovascular approach are that it remains less invasive, the risk for myocardial infarction is lower, and there is no need for general anesthesia. This patient could have received an endovascular approach with catheter-based therapies to achieve a similar outcome. Although the authors do not report what was removed from the artery, or the size of the embolus, we can surmise that it was removed with the open repair with little difficulty and was atheroembolic. Given this supposition, an endovascular approach involves the following procedures: crossing the occlusion and deploying a distal protection device (either filter or balloon occlusion) and proceeding with an aspiration/thrombectomy catheter. Given the small nature of these vessels in the forearm, my approach would be to place a distal occlusion balloon (PercuSurge, Medtronic, Inc, Minneapolis, Minnesota) in the distal brachial artery or distal vasculature. Once distal protection was achieved aspiration with the AngioJet device (Possis Inc., Minneapolis, Minnesota) or an aspiration catheter such as the Export (Medtronic, Inc.) or another similar device. An alternative therapy would be to perform laser ablative therapy to the atheroembolus. Following either, these therapies and “sump” aspiration of the distal location of the occlusion balloon perform angiography for the result. Critically, if this is atheroembolic and not thromboembolic, the urgent need for either PTA or thrombolytic therapy is low and can hamper a good final result. The critical goal of this endovascular approach is to protect the distal vasculature to avoid any further potential compromise of the hand or distal vascular beds. If after the first angiography or the subsequent post-interventional angiography the vessels do not appear patent or there is a poor result, then the “bail-out” to a surgical approach should be pursued.
How Would You Treat This Patient?
Aravinda Nanjudappa, MD,
RVT Associate Professor of Medicine and Surgery,
West Virginia University, Charleston, West Virginia Robert
S. Dieter, MD,
RVT Assistant Professor of Medicine,
Loyola University, Chicago, Illinois
As the incidence of hypertension and diabetes continues to rise, so does the increased rate of end stage renal disease (ESRD).1 Renal replacement therapy is best served by placement of native arterio-venous fistula (AVF) creation. National Kidney Foundation guidelines for native AVF creation are at least 50% of all new ESRD patients and 40% of prevalent hemodialysis patients.2 The article illustrates an example of arterial inflow disease leading to graft failure. In this case study, it is difficult to pinpoint the etiology of emboli with the aorta as the source. The emboli could have been from a juxta-anastomotic artery. Type B dissection involves aortic dissection below the subclavian artery and hence, should not affect the sublclavian artery and its branches. The presence of atherosclerosis by computed tomographic scan and echocardiogram can be incidental. The definitive signs of cardiac and aorta as sources of emboli are the presence of left ventricular thrombus and > 4 mm aorta atheroma by transesophageal echocardiography. The nature of cardiac rhythm by EKG and telemetry would be helpful. Arial fibrillation is the number one cause for cardiac source of emboli.3 The presence or absence of patent foramen ovale or atrial septal defect by echocardiography is essential to rule out the role of paradoxical embolus. The status of the valve for vegetation is helpful, as bacterial endocarditis is high among patients undergoing hemodialysis. Intracardiac valvular vegetation can embolize and cause acute hand ischemia. The treatment of embolic lesion leading to acute ischemia is definitely surgical with embolectomy. However, use of thrombolysis with active surgery can lead to hematoma, bleeding, and complications, as noted in the case. Thrombolysis is contraindicated in patients who have undergone or are undergoing surgery in less than two weeks.4 If the case was entirely performed percutaneously, (although not recommended), then arterial thrombolysis could be justified. Lastly, we assume that treating patients with atheroma with warfarin to be safe and effective. However, limited data are available, and the recommendations are provided only for aortic atheromas that are > 4 mm in size. There are case reports of increased atheroembolism following warfarin therapy in such patients and hence, statins and ACE inhibitors may have a role.5
1. Sarafidis PA, Li S, Chen SC, et al. Hypertension awareness, treatment, and control in chronic kidney disease. Am J Med 2008;121:332–340.
2. Rayner HC, Pisoni RL, Gillespie BW, et al. Dialysis outcomes and practice patterns study. Creation, cannulation, and survival of arteriovenous fistulae: Data from the dialysis outcomes and practice patterns study. Kidney Int 2003;63:323–330.
3. Murtagh B, Smalling RW. Cardioembolic stroke. Curr Atheroscler Rep 2006;8:310–316.
4. Samett EJ, Khan AN. Thrombolysis. Peripheral e medicine Jul 14, 2006.
5. Sheikhzadeh A, Ehlermann P. Atheromatous disease of the thoracic aorta and systemic embolism: Clinical picture and therapeutic challenge. Zeitschrift für Kardiologie 2004;93:10–17.