Vascular Access Emergencies in the Dialysis Patient

According to the National Institute of Diabetes and Digestive and Kidney Diseases, approximately 468,000 persons in the United States are on dialysis—a number that continues to grow annually. ¹ The 1-year rate for hemorrhagic complications from arteriovenous fistulas (AVFs) is estimated to be 0.4%. ² One study by Ellingson et al ³ reported 1,654 deaths secondary to fatal vascular access hemorrhage over a 6-year period, accounting for 0.4% of all deaths of hemodialysis (HD) patients in that study. ³

Nonhemorrhagic vascular access-related complications also contribute to the morbidity and mortality associated with AVFs and arteriovenous grafts (AVGs). Venous stenosis resulting in thrombosis has been estimated to occur in 24.7% of AVGs and 9.0% of AVFs, both of which are common causes of access failure.

Infection is reported to be the second leading cause of death in dialysis patients, and vascular access-related infection rates are reported to occur in 9.5% of AVGs vs 0.4% to 0.9% of AVFs. ^2,4 Pseudoaneurysms and aneurysms range from 30% to 60% for AVFs, ^2,5 and contribute to morbidity by limiting available areas to cannulate for dialysis, occasionally requiring surgical revision to restore access function or prevent access rupture.

Steal phenomena, including dialysis access-induced steal syndrome (DASS) and ischemic monomelic neuropathy, as well as heart failure secondary to high output are additional contributors to morbidity and mortality.

With the growing rate of end-stage renal disease (ESRD) in the United States and the contribution to morbidity and mortality by bleeding and other complications, it is essential to understand how to evaluate and treat these patients in the ED. This article reviews the evaluation and treatment of vascular access emergencies, as well as risk factors that contribute to complications in the ESRD patient population.

Hemorrhagic Complications of Vascular Access

Risk Factors

Many patients with ESRD have multiple comorbidities such as coronary artery disease and atrial fibrillation that require anticoagulation, antiplatelet medications, or both. Studies have shown that ESRD patients taking warfarin have an increase in major bleeding episodes of 3.1% per person-year and 4.4% per person-year for those taking aspirin alone, while those taking both medications have an increased bleeding risk of 6.3% per person-year. ⁶ A recent systematic review by Elliott et al ⁷ has suggested a 2-fold increase in bleeding rates in HD patients anticoagulated with warfarin as compared to HD patients not on warfarin.

While uremia secondary to chronic kidney disease (CKD) is a well-known facilitator of bleeding complications, the underlying pathophysiology is not yet completely delineated. However, there are some general underlying principles that may help in understanding the best treatment modalities available at this time. As the kidneys fail, uremic toxins accumulate in the bloodstream. These toxins include urea, creatinine, and phenolic acids, which are believed to interfere with primary hemostasis by effecting platelet adherence to endothelium, platelet activation, and aggregation. ⁸ Functional defects are created in the interactions between the glycoprotein Ib (GPIb) receptor and von Willebrand factor (vWF), which are essential to endothelial adhesion of platelets. ⁹ Additionally, these toxins impair the up regulation of the GPIIbIIIa receptor which is integral to platelet aggregation. ¹⁰ Platelet activation normally leads to platelet aggregation by increasing production of thromboxane A2 (TXA2) and serotonin that are released from storage granules. ¹⁰ Some toxins may increase nitric oxide (NO) synthesis, effectively reducing aggregation by decreasing TXA2 and adenosine diphosphate (ADP) levels. ¹¹ In addition, elevated levels of fibrinogen fragments have also recently been shown to inhibit platelet function by competing with fibrinogen for the GPIIbIIIa receptor with decreasing levels demonstrated after HD. ¹²