Hemodialysis Vascular Access Complications

Hemodialysis Vascular Access Complications

H e m o d i a l y s i s Vas c u l a r Access Complications Recognition and Management Maria Anaizza Aurora Reyna, MD a, *, Tonia Kim, MD b KEYWO...

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H e m o d i a l y s i s Vas c u l a r Access Complications Recognition and Management Maria Anaizza Aurora Reyna,



*, Tonia Kim,



KEYWORDS  Hemodialysis  Arteriovenous fistula  Arteriovenous graft  Tunneled catheters  Thrombosis  Stenosis  Steal syndrome  Ischemic monomelic neuropathy


1. Arteriovenous (AV) fistula is the vascular access of choice, and is associated with lower complication rates. 2. The use of central venous catheters for hemodialysis should be minimized, as they are associated with increased patient morbidity and mortality. 3. Physical examination can accurately detect and localize stenosis and thrombosis in AV fistulas and grafts. 4. There is no consensus supporting the routine use of either anticoagulants or antiplatelet strategies to reduce the risk of thrombosis in long-term use of vascular access. 5. Thrombosed, abandoned AV grafts may be a potential source of infection, evidence of which might not be apparent on physical examination. 6. Special attention must be paid to diabetic patients with neuropathy, as they have an increased risk of developing ischemic complications from their AV access. 7. Stenosis, access infection, aneurysm, and pseudoaneurysm are risk factors for fatal vascular access hemorrhage. 8. Patients graded New York Heart Association class III and IV who require dialysis should not have an AV fistula placed, as this can lead to high-output cardiac failure. 9. Catheter occlusion should be managed by locally instilling thrombolytic agents before exchange or replacement of catheter guide wire. CONTINUED


Division of Hospital Medicine, Mount Sinai Hospital, 1 Gustave L. Levy Place, New York, NY 10029, USA; b Division of Nephrology, Mount Sinai Hospital, 1 Gustave L. Levy Place, New York, NY 10029, USA * Corresponding author. E-mail address: [email protected]

Hosp Med Clin 3 (2014) 504–530 http://dx.doi.org/10.1016/j.ehmc.2014.06.003 2211-5943/14/$ – see front matter Ó 2014 Elsevier Inc. All rights reserved.

Hemodialysis Vascular Access Complications


10. Among dialysis patients in whom a peripheral blood sample cannot be obtained, catheter-related bloodstream infection can be diagnosed if cultures drawn from blood tubing are positive with a credible pathogen in a patient with signs and symptoms of bacteremia, but without evidence of an alternative source of infection. 11. Central venous catheters should be removed from all hemodynamically unstable dialysis patients with catheter-related bloodstream infection. 12. Use of aseptic techniques is an important step in the prevention of catheterrelated infections.


What are the different types of vascular access? The 3 basic types of vascular access for hemodialysis are an arteriovenous (AV) fistula, an AV graft, and a venous catheter (Table 1). The goal is to provide reliable sites of access to the circulation with minimal associated morbidity and mortality. EPIDEMIOLOGY

What are the incidences of complications for each type of vascular access?  Compared with individuals with fistulas, those using catheters have a 38% risk for a major cardiac event, a 53% higher risk of dying, and more than double the risk of developing fatal infections.1

Table 1 Types of hemodialysis vascular access Type



Arteriovenous (AV) fistula

Formed by anastomosing an artery directly to a vein

Hemodialysis access of choice Needs time to mature (about 6–8 wk)

AV graft

Formed by connecting an artery to a vein using a synthetic conduit, usually expanded polytetrafluoroethylene

Can be used 2–4 wk after placement Alternative for patients who are unable to have a fistula

Central venous Plastic catheter inserted into a large No maturation time Used in patients who require urgent catheter vein dialysis and for whom no other Two types: access exist 1. Nontunneled catheters  Catheter emerges from the skin at the site of entry into the vein 2. Tunneled catheters  Surgically or radiologically implanted central catheters with tunneled portion exiting the skin  Has a subcutaneous cuff for tissue ingrowth



Aurora Reyna & Kim

 Compared with individuals with fistulas, those with grafts have an 18% increased risk of dying and a 36% increased risk of developing fatal infections, but do not have an increased risk of experiencing a major heart-related event.1  AV fistulas are less likely than grafts to develop stenosis and thrombosis.2,3  Grafts are 3.8 times more likely to require a thrombectomy and 3 times more likely to require access intervention than native fistula.4  Dialysis-associated steal syndrome occurs in approximately 1% of AV fistulas and 4% to 6% of polytetrafluoroethylene grafts.5,6  Tunneled dialysis catheters are associated with lower rates of infection in comparison with nontunneled catheters.7


What is stenosis? Stenosis is defined as narrowing of blood vessels caused by neointimal hyperplasia. Progressive stenosis leads to a graduated decrease in blood flow through the access and eventual clotting within the vessel/graft, which ultimately leads to access failure and loss. What are the characteristic features of a stenosed fistula/graft? Physical examination can assist in the detection and localization of stenosis in the AV fistula and graft. Recent studies have confirmed that a good physical examination correlates well with angiographic data.8,9 An AV fistula/graft with stenosis will demonstrate an abnormal pulse, thrill, or bruit on physical examination (Table 2). A properly functioning graft/fistula has a soft compressible pulse with a continuous thrill best palpable at the arterial anastomosis. A bruit is low pitched, and decreases in pitch as one moves up the arm and the velocity of flow decreases. With the development of significant venous stenosis, upstream resistance is increased, which causes an increase in the force of the pulse within the graft/fistula below the stenosis. Narrowing within the bloodflow channel produces turbulence. The greater the turbulence, the stronger is the thrill. Both the turbulence and the thrill are localized to the site of stenotic lesion. As the degree of stenosis increases, the velocity of flow increases and the pitch of the bruit rises.10 Outflow stenosis can be further evaluated using the arm elevation test for veins and the pulse augmentation test for arteries. What is the arm elevation test? Venous outflow stenosis can be detected by physical examination using the arm elevation test. In a normal fistula or graft, having the patient raise the arm above the level of the heart should allow venous collapse and flattening of the fistula; if there is significant outflow stenosis, the portion of the fistula distal to the lesion will remain distended while the proximal portion collapses (Fig. 1). What is the pulse augmentation test? Inflow lesions from inadequate arterial flow can be assessed by physical examination using pulse augmentation. This test is performed by briefly, but completely occluding

Hemodialysis Vascular Access Complications

Table 2 Physical findings of arteriovenous access stenosis Parameter





Sudden change in pressure caused by the beat of the heart Felt using finger

Soft and compressible

Pulse not easily compressible Strong pulse (intensity of pulse is directly proportional to severity of stenosis) Palpable at stenotic site


Palpable vibration over fistula/graft that is related to blood flow Best felt using palm of hand

Felt most prominently at the arterial anastomosis; diminishes in strength as you move farther away from the anastomosis Continuous Soft, diffuse

Additional thrill felt at area of stenotic lesion


Auditory manifestation of a thrill Heard using a stethoscope

Continuous Low pitch Has diastolic and systolic component Prominent at area of anastomosis; diminishes in strength as you move farther away from the anastomosis

Discontinuous High pitch No diastolic component

the access some distance away from the arterial anastomosis while the pulse is palpated between the 2 points. The pulse over a normal graft is augmented by this maneuver. When there is substantial inflow narrowing, no such increase will be observed. The degree of this augmentation is directly proportional to the quality of the arterial inflow. How is AV fistula/graft stenosis managed? If a hemodynamically significant stenosis is suspected by physical examination and/or flow measurement, angiography should be performed as soon as possible. With angiography, a stenotic lesion is recognized by comparison with an adjacent normal vein or fistula. Stenosis of AV graft or primary AV fistula should be treated with percutaneous transluminal angioplasty (PTA) or surgical revision if stenosis is greater than 50% of the lumen diameter and is associated with hemodynamic, functional, or clinical abnormalities such as a previous thrombotic episode, abnormal physical findings, or decreased access flow.11 PTA has the advantages of being a shorter procedure than surgery and thus negating the need for prolonged hospitalization, having a lower chance of infection, sparing the patient’s veins, and, in most cases, enabling immediate dialysis without the need for a temporary central venous catheter (CVC).12 If angioplasty is required more than 2 times within 3 months, the patient should be referred for surgical revision if such an option is available and if the patient is a good surgical candidate.11



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Fig. 1. Arm elevation test. (A) Fullness (arrow) near the anastomosis resulting from a small aneurysm. The fullness collapses completely on arm elevation (B, arrow) suggesting an absence of significant outflow obstruction. (From Vachharajani T. Atlas of dialysis vascular access. Available at: http://www.fistulafirst.org. Accessed February 15, 2014; with permission.)

Arteriovenous Access Thrombosis

What is thrombosis? Thrombosis is the formation of a blood clot within an AV fistula or graft obstructing the flow of blood through the access. Thrombosis is associated with underlying venous stenosis in greater than 85% of instances.11 What are the characteristic features of a thrombosed fistula/graft? A thrombosed AV fistula/graft will have an absent pulse, no thrill, and absent bruit owing to complete loss of flow.8 How is AV fistula/graft thrombosis managed? AV graft thrombosis

Therapeutic options include percutaneous or surgical thrombectomy, thrombolytic agents, and mechanical dissolution. The choice of technique to treat thrombosis should be based on the expertise of the center.11 If these modalities are successful, a fistulogram can then be performed and detected stenoses treated with angioplasty or surgical revision. Failure to treat underlying stenosis will result in rapid repeat thrombosis.13 AV fistula thrombosis

Treatment of thrombosis in native AV fistulas requires immediate attention and treatment, in contrast to thrombosis in AV grafts. Neither percutaneous nor surgical techniques

Hemodialysis Vascular Access Complications

offer good results if treatment of AV fistula thrombosis is delayed. Each institution should attempt to resolve thrombosis with the preferred technique at that institution.14 Can antiplatelets/anticoagulants prevent arteriovenous stenosis/thrombosis? Several studies have attempted to evaluate the effect of antiplatelet agents and anticoagulants on preventing graft and fistula thrombosis; however, results have been conflicting. Most trials that show benefit of the use of antiplatelets in preventing thrombosis in arteriovenous access have had short periods of follow-up (1 month or less).15 In a study evaluating the effectiveness of aspirin plus clopidogrel versus placebo in preventing graft thrombosis, there was no difference between the 2 groups in terms of thrombosis rates (hazard ratio [HR] 0.81, 95% confidence interval [CI] 0.47–1.40; P 5 .45), and the trial was terminated early because of a 2-fold increase in bleeding events in patients treated with aspirin and clopidogrel (HR 1.98, 95% CI 1.19–3.28; P 5 .007).16 In a trial involving dipyridamole plus aspirin, treatment showed a significant but modest effect in reducing the risk of stenosis and improving the duration of primary unassisted patency of the newly created graft. There was no difference in bleeding rates in comparison with placebo. However, the decreased bleeding may be due to exclusion of patients with an increased bleeding risk and the short duration of use of the drugs.17 A clinical trial of low-dose warfarin (target international normalized ratio [INR] 1.5– 1.9) versus placebo showed no difference in graft thrombosis, and 10% of the patients receiving warfarin developed major hemorrhage despite close monitoring of the INR.18 At present, there are no data that support the routine use of antiplatelets or anticoagulants in the prevention of AV fistula/graft stenosis/thrombosis. Can supplementation with fish oil prevent AV graft thrombosis? In a randomized controlled study, daily ingestion of fish oil did not decrease the proportion of grafts with loss of patency within 12 months. However, rates of thrombosis and the need for corrective interventions were lower in the fish-oil group than in the placebo group. In addition, cardiovascular event-free survival was higher in the fishoil group and systolic blood pressure decreased to a greater extent.19 The studied cohort was limited to patients with new AV grafts. Arteriovenous Access Infection

What are the signs and symptoms of an infected AV fistula or AV graft? Patients may complain of fever, chills, and pain in the access site. Physical examination may reveal localized erythema, induration, fluctuance, exposed access, and a draining sinus tract.20 Infection can also present as bleeding from the anastomosis. How is infected AV access diagnosed? AV access infection is usually diagnosed based on physical examination. However, lack of signs and symptoms does not exclude the possibility of clinically silent graft infection. Thrombosed, abandoned grafts have been shown in several studies to pose an infectious risk that may not be apparent on physical examination. An indium scan can be used in these cases, and have been found to have sensitivity of 100% and specificity of 75% to 93%.21,22



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How is infected AV access managed? Infected AV fistula

Native AV fistula infection responds well to antibiotics. The 2006 National Kidney Foundation/Dialysis Outcomes Quality Initiative (KDOQI) guidelines recommend 6 weeks of antibiotics. Surgical excision is not warranted except in the setting of septic emboli.23 Infected AV graft

In infected grafts, local infection can be managed with appropriate antibiotics based on culture results. Duration of antibiotic treatment can vary, but most would treat for 4 to 6 weeks. If the appropriate antibiotic therapy is unsuccessful in eradicating the infection, incision and resection of the infected portion of the graft can be performed by a vascular surgeon.24 Extensive infection should be treated with total resection of the graft.25 Dialysis Access–Induced Ischemia

What is dialysis-associated steal syndrome? Dialysis-associated steal syndrome (DASS) refers to hand ischemia caused by peripheral hypoperfusion resulting from an AV fistula or synthetic vascular graft. It is more commonly seen in patients with brachial artery–based rather than radial artery–based access,26 and in diabetics and smokers.27 What is the pathophysiology of DASS? The pathogenesis of DASS is complex and poorly understood, but is thought to be related to a combination of excess blood flow through the AV fistula conduit (true steal), presence of arterial stenosis in the arm (proximal and distal) restricting blood flow to the hand, and lack of vascular (arterial) adaptation or collateral flow reserve (ie, atherosclerosis) to the increased flow demand from the AV conduit.28,29 How does DASS clinically present? DASS is a spectrum of ischemia characterized by:       

Hand pain and numbness Pale, cold hand Diminished or absent pulses Atrophy Severe neuropathy Ischemic ulcers Gangrene

DASS may appear acutely after vascular access construction, subacutely within the first few weeks, or chronically several months after AV fistula/graft placement.28 How is DASS diagnosed? Diagnosis is based on an accurate history and physical examination, and confirmed with tests including an arteriogram, duplex Doppler ultrasonography evaluation with finger pressures, and waveform analysis.29

Hemodialysis Vascular Access Complications

How is DASS managed? The primary goal is to reverse ischemia while preserving the access. A vascular surgeon should be consulted. A complete arteriogram should be done to evaluate for arterial stenosis (Fig. 2). Medical management should include diabetes control and smoking cessation.28 Surgical interventions include DRIL (distal revascularization–interval ligation) and MILLER (minimally invasive limited ligation endoluminal-assisted revision). Aggressive physical therapy is warranted after surgery. What is ischemic monomelic neuropathy? Ischemic monomelic neuropathy (IMN) is a multiple axonal-loss mononeuropathy that develops after acute arterial occlusion or low blood flow to an extremity, resulting in motor and sensory nerve dysfunction.30 What is the pathophysiology of IMN? The pathogenesis is due to hypoperfusion of the vasa nervosum. Ischemia is transient or insufficient to cause muscle or skin necrosis, but results in severe ischemic nerve injury in susceptible patients.

Fig. 2. Algorithm to treat patients with symptoms of dialysis-associated steal syndrome. MILLER, minimally invasive limited ligation endoluminal-assisted revision; PTA, percutaneous transluminal balloon angioplasty. (Adapted from Asif A, Leon C, Merrill D, et al. Arterial steal syndrome: A modest proposal for an old paradigm. Am J Kidney Dis 2006;48:88–97; with permission.)



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Patients at risk are those with long-standing diabetes with peripheral neuropathy and vascular disease. IMN only occurs with accesses placed at the antecubital position.31

How does IMN clinically present? Symptoms occur along the distribution of radial, ulnar, and median nerves.    

Decreased sensation in the fingers Allodynia/hyperesthesia Poor wrist extension and reduced thumb apposition Forearm muscles may be relatively spared compared with the intrinsic hand muscles, resulting in a profound loss of grip (claw-hand deformity)

How is IMN different from DASS? Severe neurologic dysfunction out of proportion to the degree of ischemia in the affected extremity is the hallmark of the condition, and differentiates it from DASS (Table 3). IMN occurs within hours of fistula or graft formation. The symptoms of IMN are often disabling and irreversible, but do not cause tissue necrosis.31

How is IMN diagnosed? The diagnosis is mainly made clinically. Electromyogram (EMG) and nerve conduction studies can be used to confirm the diagnosis. The EMG typically shows axonal loss, low amplitude, or absent responses

Table 3 Difference between dialysis-associated steal syndrome and ischemic monomelic neuropathy Dialysis-Associated Steal Syndrome

Ischemic Monomelic Neuropathy


Acute or chronic

Immediate, occurs minutes to hours after placement of AV access


Can occur with access placed in upper arm or forearm

Only seen with upper arm access


Decreased vascular perfusion causing global ischemia of distal extremity

Decreased vascular perfusion causing isolated neural ischemia

Tissue involved

Skin > muscle > nerve


Predominant features

Cold hand Ischemic ulcers

Absence of tissue necrosis Pain, weakness, and paralysis of muscles

Radial pulse

Diminished or absent



Reversible if treated promptly

Irreversible even with appropriate strategy and early intervention


Percutaneous transluminal angioplasty or surgery

Fistula/graft ligation or narrowing placation to reduce the blood flow in the shunt

Hemodialysis Vascular Access Complications

to the sensory and motor nerve stimulation, and relatively preserved conduction velocities.32 How is IMN treated? Treatment includes immediate correction of ischemia by fistula/graft ligation or narrowing plication to reduce the blood flow in the shunt.32,33 Medications used to treat neuropathic pain may be helpful. Diagnosis is usually delayed, and most patients will be left with residual neurologic impairment.31 VASCULAR ACCESS HEMORRHAGE

What are the risk factors for vascular access hemorrhage? Hemorrhage from a vascular access can result in life-threatening blood loss. Bleeding from dialysis access usually occurs in the presence of infection, stenosis, repeated trauma, hypertension,34 and use of anticoagulants and antiplatelet agents.35 A rapid increase in size of an aneurysm or pseudoaneurysm, the presence of ulceration, and thinning and degeneration of the skin overlying the access are signs of impending rupture and warrant an immediate surgical referral (Fig. 3). What approaches can be used to manage bleeding? The primary goal is to control bleeding and prevent exsanguination. Treatment can be divided into mechanical modalities and correction of coagulopathy (Box 1). Vascular surgery should be consulted immediately if hemorrhage cannot be quickly controlled.

Fig. 3. Brachiocephalic fistula with an aneurysm at the arterial anastomotic site. The skin overlying the aneurysm is tight and shiny. The patient needs to be referred for urgent surgical evaluation before the aneurysm ruptures. (From Vachharajani T. Atlas of dialysis vascular access. Available at: http://www.fistulafirst.org. Accessed February 15, 2014; with permission.)



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Box 1 Modalities used to manage bleeding arteriovenous access and treat coagulopathy Direct Pressure  Apply direct pressure to the bleeding point  If bleeding stops, observe the patient for 2 hours for evidence of rebleeding and to detect graft thrombosis Indirect pressure  Firm simultaneous pressure over both the arterial and venous limb of the access will often stop or slow down the bleeding Tourniquet  Pneumatic tourniquet such as a manual blood-pressure cuff is applied above the bleeding point  The cuff pressure must be higher than systolic arterial pressure to stop blood flow  May cause distal ischemia Desmopressin (dDAVP)  Releases endogenous von Willebrand factor (vWF) from storage sites36  Dose: 0.3 mg/kg in a 50-mL bolus of saline over 30 minutes intravenously; subcutaneously 0.3 mg/kg or intranasally (2 mg/kg). Onset 1 to 2 hours, duration 4 to 8 hours37  Adverse reaction: thrombotic effects, anaphylaxis, and hyponatremia (hyponatremia is rare in patients with end-stage renal disease with insignificant residual function)  One dose can lead to tachyphylaxis secondary to depletion of factor VIII and vWF from endothelial stores Cryoprecipitate  Contains Factor VIII, fibrinogen, Factor XIII, vWF, and fibronectin  Dose: 10 units of cryoprecipitate every 12 to 24 hours; should see an effect within 4 to 12 hours  Adverse reaction: anaphylaxis, volume overload, intravascular hemolysis  Risk of exposure to bloodborne pathogens such as hepatitis, human immunodeficiency virus Protamine Sulfate  If bleeding occurs in the context of heparin use  Dose: 1 mg of protamine for every 100 units of heparin given. If the heparin dose is unknown, 10 to 20 mg of protamine can be given  Contraindications: Avoid in fish allergy, caution if prior vasectomy, and caution in pulmonary hypertension and severe left ventricular dysfunction Conjugated Estrogen  Mechanism of action not well understood but may be due to decreased generation of nitric oxide  Dose: 0.6 mg/kg intravenously over 30 to 40 minutes once daily for 5 days; onset of action 6 hours; maximum effect is evident at 5 to 7 days with duration of action 14 to 21 days Packed red blood cells  Transfuse to a hematocrit higher than 30%  Reduce bleeding time through rheologic effect38

Hemodialysis Vascular Access Complications


What is high-output cardiac failure? The combination of high cardiac output with physical findings of systemic venous or pulmonary congestion is termed high-output heart failure. A high cardiac output has been described as being greater than 8 L/min or a cardiac index greater than 3.9 L/min/m2.39 What is the pathophysiology of high-output cardiac failure caused by AV fistula? After the creation of an arteriovenous fistula, blood is shunted from the high-pressure arterial side to the low-pressure venous side. The establishment of a high-flow connection between the arterial and the venous systems causes an immediate and significant drop in peripheral arterial resistance. This process can lead to sympathetic neural activation, a compensatory increase in cardiac output, and neurohormonal activation (including the renin-angiotensin-aldosterone system and vasopressin). In turn, this can cause salt and water retention. Initially the heart increases cardiac output via an increase in heart rate and stroke volume. With time, excess cardiac stimulation leads to left ventricular hypertrophy, reduction in left ventricular ejection fraction, and eventual heart failure.40 How does cardiac failure due to high cardiac output manifest? Symptoms are similar to those of low-output heart failure, including dyspnea, exercise intolerance, fatigue, and orthopnea. On examination, the patient may exhibit tachypnea, tachycardia, elevated jugular venous pulse, pulmonary rales, and peripheral edema. In high-output heart failure, patients are likely to have warm rather than cold peripheries because of low systemic vascular resistance and peripheral vasodilatation. Alternatively, the Nicoladoni-Branham sign can be elicited by brief manual compression of the AV fistula. The response to this diagnostic maneuver is an acute bradycardia and an increase in blood pressure, which occur as a result of the sudden restoration of normal blood flow to the systemic circulation coincident with the occlusion of the AV fistula. How is high-output cardiac failure diagnosed? Chest radiograph: cardiomegaly, pulmonary congestion, effusion Echocardiogram: left ventricular dilation/hypertrophy and pulmonary hypertension, preserved left ventricular ejection fraction (>45%–50%) Right heart catheterization: high cardiac output, pulmonary hypertension with normal pulmonary vascular resistance, and low to normal systemic vascular resistance How is high-output cardiac failure treated? The goal of treatment is to eliminate fluid retention and manage the underlying cause of the high-output state.  Restricting salt intake will decrease sodium retention.  Patients with high-output heart failure and severe fluid retention should restrict fluid intake to 1000 to 1500 mL/d.39



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 The use of conventional therapies for heart failure, such as angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and certain b-blockers with vasodilatory properties are likely to further reduce systemic vascular resistance, resulting in deterioration, and are contraindicated.40  Surgical techniques used to reduce yet maintain AV fistula blood flow include banding of the AV fistula or creation of a new distal anastomosis41,42; if unsuccessful, ligation is indicated.  To avoid potential worsening of heart failure, when initiating renal replacement therapy one should strongly consider peritoneal dialysis in patients with New York Heart Association (NYHA) class III and IV heart failure.43 If peritoneal dialysis is not feasible, the risks and benefits of placing an AV fistula in NYHA class III patients and nonhypotensive class IV patients should be carefully considered and discussed with the primary care physician, cardiologist, nephrologist, and vascular surgeon. HEMODIALYSIS VENOUS CATHETER COMPLICATIONS Hemodialysis Catheter–Related Bloodstream Infection

What is the incidence of catheter-related bloodstream infection associated with nontunneled catheters and tunneled catheters? Nontunneled, noncuffed hemodialysis catheters have a higher rate of infection than tunneled cuffed catheters. The incidence of catheter-related bloodstream infection (CRBSI) associated with nontunneled catheters is highest with femoral catheters, followed by internal jugular catheters and subclavian catheters.7 The placement of subclavian vein catheters often leads to development of central venous stenosis, and is generally avoided. Tunneled femoral catheters have infection-free survival similar to that of internal jugular vein catheters. However, femoral tunneled catheters have substantially shorter duration of primary catheter patency (time from initial placement to first exchange) and an increased risk of lower extremity deep vein thrombosis.44 How does hemodialysis CRBSI manifest? Fever and/or chills are the most sensitive clinical manifestation of catheter-induced bacteremia. Exit-site infection as indicated by the presence of erythema, tenderness, swelling, and purulent drainage around the catheter exit is more specific but less sensitive. Most cases of catheter-associated bacteremia occur in the absence of an exit-site infection. Other manifestations include hypotension, altered mental status, and catheter dysfunction. Elderly and more immunocompromised patients may present with hypothermia, hypoglycemia, and acidosis.22 Metastatic infectious complications, such as septic arthritis, osteomyelitis, spinal epidural abscess, infective endocarditis, and septic emboli may also occur. How is CRBSI diagnosed? The definitive diagnosis of catheter-related bacteremia requires 1 of the following45:  Growth of the same organism from at least 1 percutaneous blood culture and from a culture of the catheter tip  Concurrent positive blood cultures from the catheter and a peripheral vein, with the colony count from the catheter at least 3-fold greater than that obtained from

Hemodialysis Vascular Access Complications

the peripheral vein; alternatively, catheter cultures should become positive at least 2 hours earlier than the simultaneously drawn peripheral blood These criteria are straightforward for nondialysis patients but pose several challenges in hemodialysis patients.  Obtaining peripheral blood may not be feasible because peripheral veins have been exhausted as a result of multiple failed dialysis fistulas/grafts, or it is deemed desirable to preserve the veins intended for future vascular access creation.  If the febrile episode occurs during dialysis, when systemic blood is circulating through the catheter, it is unlikely that there may be a meaningful difference between the peripheral and catheter blood culture results. Because of these limitations, the Infectious Disease Society of America (IDSA) made provisions to accept blood cultures drawn during hemodialysis from blood lines connected to the CVC instead of from peripheral vein when a peripheral blood sample cannot be obtained. Therefore, in the absence of clinical evidence of an alternative source of infection, positive blood cultures drawn from a catheter in a patient with signs and symptoms of bacteremia should be considered a possible CRBSI and should be treated as such. Although this is only considered “possible CRBSI” by IDSA, it is an appropriate and more practical definition of hemodialysis CRBSI. What are the most common pathogens responsible for most dialysis catheter–related infections? Catheter-related bacteremia may result from a broad spectrum of gram-positive and gram-negative bacteria, but are most often due to coagulase-negative staphylococci (CONS) or Staphylococcus aureus (Box 2). Differentiating true CONS infection from contamination can be difficult. Time to blood culture positivity, quantity of growth per culture bottle, and presence of multiple positive cultures with identical antibiograms can be useful in determining whether a positive blood culture represents true infection.46,47 A substantial proportion of staphylococcal infections in dialysis patients are methicillin-resistant. Which antimicrobials should be used to treat hemodialysis catheter–related bacteremia?  Empiric treatment should include vancomycin and coverage for gram-negative bacilli, based on the local antibiogram (eg, third-generation cephalosporin, carbapenem or b-lactam/b-lactamase combination) (Table 4).  Antibiotic selection should be made based on pharmacokinetic properties that permit dosing and/or after each dialysis session to improve patient compliance and treatment efficiency; this is the case for vancomycin, ceftazidime, cefazolin, daptomycin, and aminoglycoside.  Presence of residual renal function should be considered when determining choice, dose, and frequency of antibiotics. Aminoglycosides should be avoided in gram-negative bacteremia if the patient has residual renal function and is sensitive to third-generation cephalosporins.  Once the organism and sensitivities have been identified, the antibiotic regimen should be adjusted accordingly to limit unnecessary antibiotic exposure and potential for the development of resistant organisms.



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Box 2 Select pathogens responsible for hemodialysis catheter–related bacteremia Gram-positive cocci Staphylococcus aureus Staphylococcus epidermidis Methicillin-resistant Staphylococcus aureus Enterococcus faecalis Gram-negative bacilli Pseudomonas aeruginosa Acinetobacter Escherichia coli Enterobacter Klebsiella pneumoniae Serratia marcescens Fungi Candida Acid-fast bacilli Mycobacterium tuberculosis Mycobacterium chelonae

 In particular, vancomycin should be substituted with cefazolin in patients with methicillin-sensitive S aureus bacteremia. Continued treatment with vancomycin in the case of methicillin sensitivity has been shown to substantially increase the risk of treatment failure.48 Moreover, unnecessary continuation of vancomycin therapy may promote the emergence of vancomycin-resistant infections.49 What is the appropriate duration of antimicrobial therapy for catheter-related bacteremia? Duration of antibiotic depends on whether the CRBSI is complicated or uncomplicated, and the causative agent (Fig. 4). How are infected catheters managed?  Nontunneled, noncuffed catheters should be removed in the presence of bacteremia (Fig. 5).  Removal of a tunneled catheter with delayed CVC replacement is required in: 1. Hemodynamically unstable patients 2. Presence of metastatic infection 3. Evidence of tunnel infection 4. Persistent fever/bacteremia more than 48 hours after initiating appropriate antibiotic 5. Infection caused by S aureus, Pseudomonas, fungi, and multidrug resistant pathogens

Table 4 Intravenous antimicrobial treatment of hemodialysis catheter–related bacteremia according to specific pathogen isolated Organisms


Dosing Regimen

Methicillin-resistant Staphylococcus aureus

Vancomycin If MIC vancomycin >2 mg/mL or vancomycin allergy: daptomycin

Vancomycin: 20 mg/kg loading dose infused Vancomycin trough levels should be monitored to avoid toxicity and subtherapeutic levels during the last hour of the dialysis session, that can lead to antibiotic resistance then 500 mg during the last 30 min of each Target trough level for bacteremia: 15–20 mg/mL subsequent dialysis session

Methicillin-sensitive Staphylococcus

Nafcillin 12 g/24 h in 4–6 divided doses Penicillinase-resistant penicillin (eg, nafcillin) or a first-generation Cefazolin: 20 mg/kg IV after each dialysis session cephalosporin (eg, cefazolin) Penicillin allergy: vancomycin

Daptomycin: 6 mg/kg after each dialysis session

Gram-negative Bacteria

Third-generation cephalosporin or aminoglycoside or carbapenem

Ceftazidime: 1 g IV after each dialysis session Gentamicin (or tobramycin): 1 mg/kg, not to exceed 100 mg after each dialysis session


Echinocandin, fluconazole, or amphotericin B

Caspofungin: 70 mg IV loading dose followed by 50 mg IV daily Micafungin: 100 mg IV daily Anidulafungin: 200 mg IV loading dose followed by 100 mg IV daily Fluconazole: 200 mg orally daily

Cefazolin is preferred because it can be administered after each dialysis session Nafcillin is administered every 4 to 6 h and usually entails placement of a PICC, which should be avoided in dialysis patient as it produces rapid thrombosis of veins, jeopardizing future creation of a permanent access in the ipsilateral arm If nafcillin is required, a Hickman catheter can be placed instead of a PICC

Gentamicin can cause ototoxicity and vestibulotoxicity in dialysis patients Gentamicin levels should be monitored: Ideal peak level for bacteremia: 6–12 mg/mL Ideal trough level: <2 mg/mL

Abbreviations: IV, intravenous; MIC, minimum inhibitory concentration; PICC, peripherally inserted central catheter.

Hemodialysis Vascular Access Complications

Vancomycin-resistant Daptomycin Enterococcus




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Fig. 4. Catheter management and antibiotic duration based on microorganisms causing catheter-related bloodstream infection. abx, antibiotics.

 For patients who lack these indications for removal or for whom removal of a cuffed catheter is not feasible or practical, the infected catheter can be exchanged over a guide wire with a new catheter. Studies suggest that this approach is associated with cure rates similar to those of immediate catheter removal and delayed replacement, while reducing the number of access procedures required.50–52  An alternative approach is to use an antibiotic lock as adjunctive therapy to systemic antibiotics in patients without indications for immediate removal of the infected catheter. There have been no well-defined prospective comparative studies that have examined the efficacy of antibiotic lock therapy versus guide-wire exchange.  With both guide-wire exchange and antibiotic lock, the infected catheter is removed if fever and bacteremia persists.  Surveillance blood cultures should be obtained 1 week after completion of an antibiotic course for CRBSI if the catheter has been retained.

Hemodialysis Vascular Access Complications

Fig. 5. Approach to patient with hemodialysis catheter-related bloodstream infection. MDR, multidrug resistance.

 There is no role for leaving the infected catheter in place without either instilling an antibiotic lock or replacing the infected catheter. Administration of intravenous antibiotic alone is unsatisfactory because bacteremia recurs when the course of antibiotics has been completed.53–55 What is antibiotic lock therapy and how is it used to manage patients with catheterrelated infection? If removal of the catheter is deemed undesirable or impossible, antibiotic lock is an important therapeutic option. This lock consists of a very high concentration of



Aurora Reyna & Kim

antibiotics, approximately 100-fold greater than therapeutic plasma concentrations. The antibiotic lock is instilled into each catheter lumen at the end of each dialysis session for the duration of the systemic antibiotic. The goal is to sterilize the catheter lumen so that the catheter can be salvaged. Antibiotic locks should not be used alone but always in conjunction with systemic antibiotics for the recommended periods. The success rate varies considerably by organism, with 87% cure rate for gramnegative infections, 75% for Staphylococcus epidermidis infections, and 60% for Enterococcus. The success rate of salvage in the case of S aureus is low (w40%) and therefore should be considered only in problematic cases.56–58 What can be done to reduce incidence of infection? Aseptic technique  Both the Centers for Disease Control and Prevention (CDC) and KDOQI 2006 recommend scrubbing catheter hubs with an appropriate antiseptic after the cap is removed and before access, and using an alcohol-based chlorhexidine (>0.5%) solution for skin antisepsis during central-line insertion and dressing changes.59,60  Dressings for tunneled catheters have been recommended by both CDC and KDOQI. Although the CDC suggests dressings may not be necessary for wellhealed tunneled catheters, there is no particular dressing type that has shown benefit over others.61,62 Topical Antimicrobial Agents  Use of topical antimicrobial agents has been associated with decreased rates of bloodstream infections and catheter removal.62,63  KDOQI has recommended the use of either mupirocin ointment or povidoneiodine ointment at CVC exit sites after catheter placement and at the end of each hemodialysis session. The CDC has recommended povidone-iodine and not mupirocin, owing to concerns about inducing mupirocin resistance.  Ingredients in antibiotic and povidone-iodine ointments may interact with the chemical composition of certain catheters. The CVC manufacturer’s recommendations should be consulted before the use of any topical ointment at the exit site. Antibiotic Lock  The use of antibiotic locks has been associated with decreased rates of catheterrelated bacteremia and exit-site infection.63 However, several issues remain concerning, including development of antibiotic-resistant organisms from prolonged use of antibiotic and development of systemic toxicity from leakage of these solutions.  The use of antibiotic locks for the prevention of catheter-related bacteremia has not yet been approved by the Food and Drug Administration. The CDC does not currently recommend them for routine use in hemodialysis catheters, and no specific recommendation has been made by KDOQI. Hemodialysis Catheter Thrombosis

When should one suspect catheter thrombosis? When catheter dysfunction occurs immediately after insertion, it is usually due to improper placement with poor tip positioning or subcutaneous kinking of the catheter. However, if a catheter that has previously functioned in an optimal fashion begins to develop flow problems, a thrombus is likely.

Hemodialysis Vascular Access Complications

Catheter malfunction is defined as failure to attain and maintain an extracorporeal blood flow sufficient to perform hemodialysis treatment without significantly lengthening the hemodialysis treatment. Sufficient extracorporeal blood flow is considered to be 300 mL/min.64 What are the different types of catheter thrombosis? Catheter-associated thrombosis can be classified as extrinsic and intrinsic. Intrinsic thrombosis occurs when a thrombus forms within the catheter lumen or completely surrounds it (Table 5). It results from either an inadequate volume of heparin being placed within the catheter lumen, heparin being lost from the catheter between dialysis treatments, or the presence of blood in the catheter. An extrinsic thrombus is one that forms outside of the catheter (Table 6). How is an intrinsic thrombus treated? Low blood flows within a catheter may be corrected by forceful saline flush. A 5- to 10mL saline-filled syringe is attached to the catheter, and the saline is forcibly flushed into the catheter and aspirated. Saline flush can be repeated several times until blood is aspirated and flow appears free and easy. When this is not successful, malfunctioning catheters can be treated empirically by local intracatheter instillation of a thrombolytic agent by hemodialysis staff. Urokinase historically was the agent of choice for this purpose, but was withdrawn from the United States market because of a viral contamination. Streptokinase should not be used because of the risk of allergic reaction.65 At present, the tissue plasminogen activator (tPA) alteplase is the only thrombolytic agent approved for CVC thrombus clearance. The benefit from this tPA is short lived, with a median time of about 27 days before requiring another thrombolytic instillation.66 If malfunction persists, the catheter should be exchanged over a guide wire. In the case of fibrin sheath, the preferred intervention as per KDOQI guidelines is removal of the catheter over a guide wire, disruption of the sheath with an angioplasty balloon, and placement of a new catheter. How is an extrinsic thrombus treated? Treatment consists of catheter removal and 3 months of anticoagulation for central vein and mural thrombus.67 However, treatment varies depending on the extent of the thrombus and the clinical setting. There have been no controlled studies to define the optimal management of a right atrial thrombus. Proposed management strategies are based on anecdotal reports and case series. Systemic anticoagulation, surgical thrombectomy, and thrombolysis are reported treatment options. All modalities should be combined Table 5 Types of intrinsic thrombosis Type



Catheter tip thrombosis

Thrombus that forms on the tip of the catheter

Inability to infuse and/or withdraw blood

Fibrin sheath thrombosis

Thrombus that surrounds the catheter as a sleeve

Inability to infuse and/or withdraw blood

Intraluminal thrombosis

Thrombus that forms within the catheter lumen

Inability to infuse and/or withdraw blood



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Table 6 Types of extrinsic thrombosis Type



Central vein thrombosis

Thrombus within the central veins, commonly the subclavian

Swelling, tenderness, or pain of the ipsilateral extremity

Mural thrombus

Thrombus that is attached to the wall of the vessel or the atrium at the point of contact by the tip of the catheter

Inability to withdraw blood Signs/symptoms of pulmonary embolism, septicemia, endocarditis

Atrial thrombus

Thrombus in the right atrium

Signs/symptoms of pulmonary embolism, septicemia, endocarditis

with removal/replacement of CVC after an initial period of anticoagulation. When changing a catheter through a guide wire, it is recommended that the catheter tip be placed in the vena cava, as formation of right atrial thrombus is thought to be associated with mechanical irritation of the right atrial endocardium.68 Stavroulopoulos and colleagues69 proposed a management algorithm based on retrospective analysis of all reported cases of catheter-related atrial thrombus (Fig. 6). In their study, there appears to be no difference in mortality whether patients are treated medically or surgically. Because of similar efficacy, anticoagulation is proposed as a first-line treatment if not contraindicated. Surgical embolectomy is indicated when the patient cannot undergo anticoagulation, thrombus is infected or its size is greater than 60 mm, or when there are cardiac abnormalities or complications that can be corrected simultaneously with surgical embolectomy. For patients who are poor surgical candidates or have contraindications to thrombolysis, percutaneous mechanical thrombectomy can be performed. Can antiplatelets and anticoagulants be used to prevent catheter thrombosis? There is insufficient evidence to recommend the routine use of warfarin to prevent tunneled cuffed catheter thrombosis in all dialysis patients, primarily because of safety concerns. Prophylactic warfarin has been shown to decrease the rate of thrombosis in patients with tunneled dialysis catheters. However, bleeding complications are increased.70 In addition, there is increasing knowledge that the use of warfarin in dialysis patients may promote vascular calcification.71,72 Use of warfarin for catheter thrombosis prophylaxis is not a routine practice. Of the commonly available antiplatelet agents, neither acetylsalicylic acid nor dipyridamole have shown consistent efficacy in preventing tunneled cuffed catheter thrombosis. Clopidogrel has not been systematically studied.73 PROCESS IMPROVEMENT

In 2003, the Centers for Medicare and Medicaid Services (CMS) and the End-Stage Renal Disease (ESRD) Networks jointly formed and implemented a national vascular access improvement initiative called the Fistula First Breakthrough Initiative (FFBI). The primary goal was to increase the appropriate use of AV fistulas and to reach or exceed the KDOQI practice guidelines. Since inception, AV fistula prevalence increased from 32% in 2003 to greater than 60% in 2011, with associated decrease in AV graft utilization.74 However, FFBI had less impact on catheter use. According to the 2013 annual data report from United States Renal Data System, nearly 80% of incident patients initiated hemodialysis therapy with CVC in 2011, with 52%

Hemodialysis Vascular Access Complications

Fig. 6. Management algorithm in the case of catheter-associated right atrial thrombus in hemodialysis patients. AC, anticoagulation; INR, international normalized ratio. a If the thrombus is 6 cm or larger but the patient is unsuitable for surgical thrombectomy, consider anticoagulation or thrombolysis treatment. b Consider lifelong anticoagulation in the case of hypercoagulable states, especially if the patient continuously receives dialysis through a catheter. (Modified from Stavroulopoulos A, Aresti V, Zounis C, et al. Right atrial thrombi complicating hemodialysis catheters. A meta-analysis of reported cases and a proposal of a management algorithm. Nephrol Dial Transplant 2012;27:2936–44; with permission.)

remaining on CVCs 90 days later. Rates of hospitalization for infection in the hemodialysis population also increased 43% from 1993 to 2011.75 Accordingly, in May of 2013 the ESRD Network Coordinating Center (NCC) launched the Fistula First Catheter Last (FFCL) Workgroup Coalition project, building on the foundation of the change concepts and success of the FFBI, but with an emphasis on decreasing the use of tunneled dialysis catheters as long-term vascular access. The goal of the initiative is to increase AV fistula prevalence to 68% and decrease long-term catheter use to less than 10%.



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Both initiatives call for modification of hospital systems to detect chronic kidney disease and promote AV fistula planning and placement. Hospitals are asked to develop a comprehensive plan for early identification and appropriate referral of patients with kidney disease while hospitalized, discharge planning that promotes AV fistula placement, and vessel preservation. GUIDELINES

National Kidney Foundation Kidney Disease Outcomes Quality Initiative. Clinical practice guidelines for 2006 updates: hemodialysis adequacy, peritoneal dialysis adequacy, and vascular access. Clinical Practice Guidelines for the Diagnosis and Management of Intravascular Catheter-Related Infection: 2009 Update by the Infectious Diseases Society of America. CDC Guidelines for the Prevention of Intravascular Catheter-Related Infections, 2011. REFERENCES

1. Ravani P, Palmer SC, Oliver MJ, et al. Associations between hemodialysis access type and clinical outcomes: a systematic review. J Am Soc Nephrol 2013;24(3):465–73. 2. Maya ID, Oser R, Saddekni S, et al. Vascular access stenosis: comparison of arteriovenous grafts and fistulas. Am J Kidney Dis 2004;44(5):859–65. 3. Allon M, Robbin ML. Increasing arteriovenous fistulas in hemodialysis patients: problems and solutions. Kidney Int 2002;62(4):1109–24. 4. Young EW, Dykstra DM, Goodkin DA, et al. Hemodialysis vascular access preferences and outcomes in the Dialysis Outcomes and Practice Patterns Study (DOPPS). Kidney Int 2002;61(6):2266–71. 5. Goff CD, Sato DT, Bloch PH, et al. Steal syndrome complicating hemodialysis access procedures: can it be predicted? Ann Vasc Surg 2000;14(2):138–44. 6. Morsy AH, Kulbaski M, Chen C, et al. Incidence and characteristics of patients with hand ischemia after a hemodialysis access procedure. J Surg Res 1998; 74(1):8–10. 7. Weijmer MC, Vervloet MG, ter Wee PM. Compared to tunnelled cuffed haemodialysis catheters, temporary untunnelled catheters are associated with more complications already within 2 weeks of use. Nephrol Dial Transplant 2004;19:670–7. 8. Asif A, Leon C, Orozco-Vargas LC, et al. Accuracy of physical examination in the detection of arteriovenous fistula stenosis. Clin J Am Soc Nephrol 2007;2(6): 1191–4. 9. Leon C, Orozco-Vargas LC, Krishnamurthy G, et al. Accuracy of physical examination in the detection of arteriovenous graft stenosis. Semin Dial 2008;21(1): 85–8. 10. Beathard G. Physical examination: the forgotten tool. In: Gray R, editor. Dialysis access: a multidisciplinary approach. Philadelphia: Lippincott Williams and Wilkins; 2002. p. 111–8. 11. NKF-K/DOQI Clinical Practice Guidelines for Vascular Access. Clinical practice guideline 21: treatment of thrombosis and associated stenosis in dialysis AV graft. Am J Kidney Dis 2006;48(Suppl 1):S248. 12. Tang S, Lo CY, Tso WK, et al. Percutaneous transluminal angioplasty for stenosis of arteriovenous fistulae: a review of local experience. Hong Kong Med J 1998;4: 36–41.

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55. Ashby DR, Power A, Singh S, et al. Bacteremia associated with tunneled hemodialysis catheters: outcomes after attempted salvage. Clin J Am Soc Nephrol 2009;4:1601–5. 56. Poole CV, Carlton D, Bimbo L, et al. Treatment of catheter-related bacteremia with an antibiotic lock protocol: effect of bacterial pathogen. Nephrol Dial Transplant 2004;19:1237–44. 57. Maya ID, Carlton D, Estrada E, et al. Treatment of dialysis catheter-related Staphylococcus aureus bacteremia with an antibiotic lock: a quality improvement report. Am J Kidney Dis 2007;50:289–95. 58. Peterson WJ, Maya ID, Carlton D, et al. Treatment of dialysis catheter-related Enterococcus bacteremia with an antibiotic lock: a quality improvement report. Am J Kidney Dis 2009;53:107–11. 59. National Kidney Foundation Kidney Disease Outcomes Quality Initiative. Clinical practice guidelines for 2006 updates: hemodialysis adequacy, peritoneal dialysis adequacy, and vascular access. Am J Kidney Dis 2006;48:S1–322. 60. O’Grady NP, Alexander M, Burns LA, et al. Guidelines for the prevention of intravascular catheter-related infections, 2011. Atlanta (GA): Centers for Disease Control and Prevention (CDC); 2011. p. 83. 61. Gillies D, Carr D, Frost J, et al. Gauze and tape and transparent polyurethane dressings for central venous catheters. Cochrane Database Syst Rev 2003;(3):CD003827. 62. McCann M, Moore ZE. Interventions for preventing infectious complications in haemodialysis patients with central venous catheters. Cochrane Database Syst Rev 2010;(1):CD00698. 63. Rabindranath KS, Bansal T, Adams J, et al. Systematic review of antimicrobials for the prevention of haemodialysis catheter related infections. Nephrol Dial Transplant 2009;24(12):3763–74. 64. Vascular Access 2006 Work Group. Clinical practice guidelines for vascular access. Am J Kidney Dis 2006;48(Suppl 1):S176–285. 65. Welik RA, Josselson J, Shen SY, et al. Repeated low-dose streptokinase infusions into occluded permanent, central-venous, hemodialysis catheters. Kidney Int 1987;31:1210–2. 66. Little MA, Walshe JJ. A longitudinal study of the repeated use of alteplase as therapy for tunneled hemodialysis function. Am J Kidney Dis 2002;39: 86–91. 67. Schwab S, Beathard G. The hemodialysis catheter conundrum: hate living with them but can’t live without them. Kidney Int 1999;56:1–17. 68. Ghani MK, Boccalandro F, Denktas AE, et al. Right atrial thrombus formation associated with central venous catheters utilization in hemodialysis patients. Intensive Care Med 2003;29:1829–32. 69. Stavroulopoulos A, Aresti V, Zounis C. Right atrial thrombi complicating haemodialysis catheters. A meta-analysis of reported cases and a proposal of a management algorithm. Nephrol Dial Transplant 2012;27:2936–44. 70. Wilms L, Vercaine LM. Does warfarin safely prevent clotting of hemodialysis catheters? A review of efficacy and safety. Semin Dial 2008;21(1):71–7. 71. Reynolds JL, Joannides AJ, Skepper JN, et al. Human vascular smooth muscle cells undergo vesicle-mediated calcification in response to changes in extracellular calcium and phosphate concentrations: a potential mechanism for accelerated vascular calcification in ESRD. J Am Soc Nephrol 2004;15:2857–67. 72. Danziger K. Vitamin K dependent proteins, warfarin and vascular calcification. Clin J Am Soc Nephrol 2008;3:1504–10.



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73. Besarab A, Pandey R. Catheter management in hemodialysis patients. Clin J Am Soc Nephrol 2011;6:227–34. 74. Vassalotti JA, Jennings WC, Beathard GA, et al. Fistula First Breakthrough Initiative: targeting catheter last in fistula first. Semin Dial 2012;25(3):303–10. 75. U.S. Renal Data System. USRDS 2013 annual data report: atlas of chronic kidney disease and end-stage renal disease in the United States. Bethesda (MD): National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2013.