In-Depth Reviews Catheter Management in Hemodialysis Patients: Delivering Adequate Flow Anatole Besarab and Rahul Pandey Summary Over 330,000 individuals in the United States depend on hemodialysis (HD), the majority as a result of end- stage renal disease. Sustainable vascular access can be achieved through arteriovenous fistulas, arteriovenous Division of Nephrology grafts, or tunneled catheters. Tunneled dialysis catheters (TDCs) often remain in use for months or even and Hypertension, years, long beyond their initial intended use as a bridging device. Research efforts are focused on identifying Department of strategies to prevent/minimize the risk of the most common catheter-related complications: thrombotic oc- Medicine, Henry Ford clusion and infection. Thrombotic occlusion of TDCs prevents adequate dialysis but can be managed success- Hospital, Detroit, Michigan fully through thrombolytic agents to restore/improve blood flow in the majority of patients, allowing immedi- ate HD delivery and prolonging usability of the TDC. Occasionally, catheter exchange with fibrin sheath Correspondence: disruption is needed to preserve the site. Surface-treated catheters could improve the morbidity and mortality Dr. Anatole Besarab, associated with HD delivery via an indwelling catheter, but results from studies have been disappointing to Division of Nephrology date. We review the etiology of catheter-based access failure and the monitoring and interventional steps that and Hypertension, should be taken to maintain the patency and safety of catheters for HD. Wherever possible we note the areas Department of Medicine, Henry Ford Hospital, in which there is scant data where further randomized clinical trials are needed. 2799 West Grand Clin J Am Soc Nephrol 6: 227–234, 2011. doi: 10.2215/CJN.04840610 Boulevard, Detroit, MI 48202. Phone: 313-916- 2713; Fax: 313-916- 2554; E-mail: abesara1@ Introduction den (13,14). A retrospective analysis of resource use hfhs.org Hemodialysis (HD) is a life-saving and life-sustaining among 88 HD patients found that 51% experienced at procedure. In 2006, approximately 330,000 individu- least one access-related complication during fol- als in the United States were receiving HD (1). Sus- low-up (mean 487 days) (15). A follow-up of 674 tainable vascular access providing high-volume blood patients from 22 chronic HD units showed a signifi- flow rates (Qb) Ͼ300 ml/min is essential, either cant association between decreased dialysis adequacy through permanent arteriovenous access or tunneled and increased hospitalization because of complica- dialysis catheters (TDCs) (2). The majority of patients tions (11%), number of hospital days (12%), and in- begin HD with a TDC (3). In the United States, 60 to patient expenditure (US$940) (16). Of all accesses, 82% of incident HD patients start with a catheter (4,5). TDCs produce the majority of problems related to Up to 33% of patients in Canada are dialyzing with a delivering adequate blood flow for dialysis and re- long-term TDC (6). quire the most interventions (2,5). TDCs allow immediate vascular access, are initially almost always functional, require no venipunctures, Defining Access Dysfunction rarely produce hemodynamic consequences, and do The 2006 National Kidney Foundation Kidney Di- not require surgical placement (7). Despite efforts to alysis Outcomes Quality Initiative (KDOQI) guide- limit their use, TDCs often remain in use for months lines define access dysfunction as the inability to or even years (8). Studies have shown that approxi- achieve Qb of Ն300 ml/min (2) during the first 60 mately 40% of patients had TDCs 90 days after com- minutes of HD despite at least one attempt to improve mencing HD (5,9,10). flow. Since then, larger bore catheter design allows Proper catheter management to preserve patency much higher Qb (Ͼ400 ml/min) to be achieved at the and to prevent/minimize the risk of infection is vital same prepump pressure. Waiting until Qb declines to in improving patient outcomes (11). This article fo- 300 ml/min in these catheters may be inappropriate, cuses on the first of these, reviewing the etiology of missing the opportunity to detect catheter dysfunc- inadequate blood flow delivery and discussing the tion earlier. However, studies to support this hypoth- monitoring and interventional steps needed to main- esis are needed. tain the patency and usability of HD catheters. Causes of Occlusive Access Dysfunction Access Dysfunction Early identification of catheter dysfunction enables The consequences of blood flow access dysfunction prompt intervention and salvage. Catheter occlusion, in HD can vary from inadequate dialysis dose deliv- a main cause of poor Qb, may be caused by kinking or ery to increased mortality (1,12). Access dysfunction malpositioning (17). In these cases, catheter dysfunc- increases resource utilization and healthcare-cost bur- tion generally emerges during the first HD session www.cjasn.org Vol 6 January, 2011 Copyright © 2011 by the American Society of Nephrology 227 228 Clinical Journal of the American Society of Nephrology and can be resolved by repositioning or, occasionally, excess of the endogenous fibrinolytic system’s capac- replacing the catheter. In a previously well function- ity develops, catheter thrombosis occurs. ing long-term catheter, inadequate flow may result from a change in position of the catheter tip during Monitoring for Access Dysfunction that session and respond to simply placing the patient Prompt identification of access dysfunction, a key in a recumbent position or adjusting the patient’s goal of the KDOQI guidelines (24), enables appropri- neck position. ate intervention (pharmacologic or mechanical) be- However, thrombotic occlusions, of which there are fore the emergence of access- and life-threatening four major types (Table 1) are a more serious cause of complications. Prospective monitoring for catheter access dysfunction. They occur in 30 to 40% of pa- Qb dysfunction should be a routine part of the med- tients, can occur within 24 hours after insertion or ical management of patients undergoing HD. Poten- after prolonged continuous successful usage (18), and tially dysfunctional catheters and reduction of Qb to can provide a substrate for bacterial growth (19). A “critical” levels can be detected before “emergency” study of 721 HD patients revealed that clot formation problems arise through systematic monitoring of Qb was one of four parameters, significantly (P Ͻ 0.001) and prepump negative arterial pressure (Pa) during and independently related to inadequate dialysis HD. The catheter channel is a long tube whose diam- dose delivery (20). eter and length determine resistance to flow (25). There is a curvilinear relationship between pressure Pathophysiology of Catheter Dysfunction and flow; the prepump pressure is virtually a nega- Injury to the vessel endothelium begins with inser- tive mirror of the venous pressure at Qb from 50 to tion of the catheter and is augmented by turbulent 500 ml/min (Figure 1a). Most large-gauge catheters flow around the catheter. “Line” reversal or catheter have a conductance (Qb/Pa) of 2 ml/min/mmHg. ”manipulation” as attempts to improve blood flow When examined serially over time at a prescribed Qb promote even more disruption in the fibrinolytic sys- (e.g. 350 to 450 ml/min), increasing negative prepump tem, initiating the coagulation and inflammatory cas- pressure to achieve the prescribed flow reflects alter- cade (21). Minute irregularities on the catheter poly- ations in inlet orifice TDC function. mer surface permit platelet adhesion and activation of We recommend the measurement of Qb at a preset the intrinsic coagulation pathway (17). Silicone may prepump pressure (e.g. Ϫ250 Ϯ 10 mmHg at each HD have less throbogenic potential than other materials (22). session 5 minutes after the start of each HD session It is the development of a fibrin sheath that deter- with trending over time. A Qb decline of Ͻ10% at the mines the long term patency of a catheter. This sheath, same negative prepump pressure may result from initially composed of fibrinogen, albumin, lipopro- many factors, but a change Ͼ10%, particularly if pro- teins, and coagulation factors, begins to form within gressive, i.e. lower conductance, suggests impending 24 hours of insertion (23). The fibrin sheath attracts access dysfunction, which may warrant intervention platelets and coagulation factors and promotes leuko- (Figure 1b). cyte adherence (21). Over weeks and months, collagen Qb decline to Ͻ300 ml/min during the first and/or is deposited as smooth muscle cells from the venous last 30 minutes of an HD session, delivered Kt/V of vessel wall migrate toward the tip. The rate of these Ͻ1.2, Pa more negative than 250 mmHg, and venous processes varies among patients because of inherited pressure of Ͼ250 mmHg are other signs of dysfunc- or acquired characteristics. Ultimately, if clotting in tion. Routine monitoring of these parameters with Table 1. Types of thrombotic occlusions Type Features Symptoms Fibrin tail or flap Fibrin extends from the end of the Ability to infuse but not catheter causing partial occlusion withdraw blood (fibrin tail acts as one-way valve) Fibrin sheath Fibrin adheres to the external surface Inability to infuse and/or encasing the catheter, possibly withdraw blood extending the length of the catheter; thrombi trapped between sheath and catheter tip Mural thrombus Fibrin from vessel wall injury binds to Leakage of infusate from the fibrin-covered catheter; increased insertion site, swelling, risk of venous thrombosis pain, tenderness, engorged vessels Intraluminal Fibrin forms inside catheter lumen Inability to infuse and/or thrombus causing partial or complete withdraw blood occlusion Clin J Am Soc Nephrol 6: 227–234, January, 2011 Hemodialysis Catheter Flow, Besarab and Rahul 229 a) the end of dialysis had deranged clotting 1 hour after 250 200 completion of dialysis. Heparinized saline, using a 150 lower total dose of heparin per catheter lumen, sig- Pv 100 nificantly reduced this rate. A lower-concentration 50 (1000 versus 10,000 U/ml) heparin lock was associated 0 with a higher use of tissue plasminogen activator -50 (tPA) (35).