Pseudoaneuryms are usually caused by hematoma development after needle puncture or in juxta-anastomic segments postoperatively. Pseudoaneurysms do not have a true wall and may secondarily become infected. 59 Pseudoaneurysms occur more frequently in AVG, and are usually reported along with true aneurysms. One study by Al-Thani et al 60 detected pseudoaneurysms in 15% of clinically significant aneurysms.
Approximately 30% to 60% of patients with AVFs will develop an aneurysm. 2,5 One study by Al-Thani et al 60 reported the need for surgical intervention in 31% of patients with an AVF in whom an aneurysm was detected. The risk for developing an aneurysm is highest for those patients on high flux membrane type HD and polycystic kidney disease. 5 As discussed earlier in this article, cannulation sites and techniques may also influence aneurysmal changes in the fistula. Aneurysm formation at the site of previous cannulation site should not be re-cannulated. 18 Aneurysmal changes can contribute to other complications including high-output heart failure, thrombosis with fistula or graft failure, increased risk of bleeding, ineffective HD when associated with thrombosis or stenosis, pain and peripheral neuropathies secondary to compression of nearby nerves, and interference with functional HD.
Many asymptomatic aneurysmal changes to vascular access may not compromise access function. If a patient is identified with a vascular access pseudoaneurysm or aneurysmal changes with high-risk features, early referral to vascular surgeon for surgical interventions is imperative. High-risk features include any of the complications previously discussed—infection, threatened overlying skin, or shiny appearance. The EP should consider duplex imaging to assist with evaluation. Treatment may include ligation of the AVF, partial resection, stenting, or grafting of the aneurysm with hopes of salvaging the vascular access. 61,62
Ischemic Monomelic Neuropathy
Ischemic monomelic neuropathy may result secondary to a type of steal phenomenon, thereby inducing ischemia to supplied nerves. Ischemic monomelic neuropathy has been described in many case reports and narrative reviews. 63-67 It has been described as ischemia or infarction of the blood supply to the nerves (vasa nervosa) in the lower arm. 68 Ischemic monomelic neuropathy typically occurs immediately after the vascular access creation in the postoperative period. Therefore, it is unlikely to be seen in the ED but as patients may have sequelae of this complication, EPs should be aware of its existence. Patients with ischemic monomelic neuropathy will have severe pain, paresthesia, and weakness immediately after placement of a vascular access. Patients also typically have sensorimotor deficits in the radial, ulnar, and median nerves. Pulses should be preserved. Severe neuropathic pain will develop and may limit the examination. Clinical diagnosis may be difficult immediately after surgery because patients will often have minor deficits secondary to the surgical procedure itself or secondary to the regional block provided by anesthesia, but nerve-conduction studies usually reveal the diagnosis. The treatment is ligation of the access immediately and prognosis is variable, depending on the severity and duration of ischemia, and may result in complete loss of function of the hand.
Steal Syndrome
Dialysis access-associated steal syndrome is a type of distal ischemia secondary to the vascular access site with a reported incidence of 6.2%, and appears to occur more frequently in AVF than AVGs. 69,70 Diabetes appears to be a strong risk factor for developing DASS. 71 Patients with DASS can present with classic ischemic symptoms such as pain, paresthesia, claudication, pallor, and diminished or absent arterial pulse. Pain may be present only while undergoing dialysis or exercising, or symptoms may be persistent. 68,72 There are several possible causes of DASS, including arterial occlusion or insufficiency proximal or distal to the anastomosis, increased flow through the conduit (true steal), or increased flow diverted through collateral vessels. 73,74 One clue to the diagnosis is a diminished or absent radial pulse that should improve with compression of the access site.
