Fig. 1. The right internal jugular (RIJ) vein is the preferred access site because it is the straightest route allowing the highest blood flow (>300 mL/min). Femoral access is a reasonable alternative with no particular preference between right- (RF) or left-sided (LF) insertion. The subclavian (Scl) approach should be avoided.
Catheter Colonization and Infection Risk
Causal analysis of 20,000 catheter days demonstrated no difference in catheter-related infection between the RIJ and the femoral site. When stratifying to body mass index, a higher femoral catheter colonization rate was observed in the highest body mass index tercile [8].
Catheter Dysfunction
Choice of vascular access site, catheter design, and competence of nursing staff in assuring correct circuit priming and monitoring, are all essential determinants of circuit survival [9, 10]. Early catheter dysfunction usually results from inadequate positioning (e.g., insertion in the wrong vessel, malposition of the catheter tip, catheter kinking) but may also be seen with strictures and hypovolemia [9, 10]. Late catheter dysfunction is most often due to thrombosis [9, 10]. Poor access causes blood flow reduction in the circuit leading to premature circuit clotting [9, 10]. The left internal jugular vein has a more tortuous path, which can lead to inadequate blood flow and early filter dysfunction [9, 10]. The subclavian access enhances the risk of catheter kinking and should be reserved for placing silicone catheters for chronic dialysis [1–3]. Femoral veins, though easily accessible in case of emergent resuscitation, do impair patient’s mobility and nursing care [11]. Low central venous pressure, high abdominal pressure, and high or very negative thoracic pressures may all result in a decreased catheter flow.
Catheter Lock
When not in use, the CRRT catheter should be locked either by controlled saline infusion or by heparin or citrate provision to prevent fibrin adhesion [11]. A 30% citrate solution guarantees optimal patency of the catheter at the lowest bleeding risk. It also reduces the risk for Staphylococcus and Candida catheter sepsis by inhibiting biofilm formation inside the catheter [12].
Fig. 2. Clinical algorithm to avoid early clotting of continuous renal replacement therapy (CRRT; adapted and modified from Gainza et al. [16] with permission) [9]. UFH, unfractionated heparin; AT III, anti-thrombin III; aPTT, activated partial thromboplastin time; INR, internationalized ratio; DIC, disseminated intravascular coagulopathy; ACD, anticoagulant citrate dextrose. AT III level above 60%. aPTT between 45 and 55 s. Prostacyclin always in association with UFH at a 5 times lower dose (1–2 U/kg/h).
Anticoagulation
A Paradigm Shift in Anticoagulation Approach
Anticoagulation is crucial for CRRT practice. Premature CRRT failure due to early clotting is a frustrating experience that reduces treatment efficacy and increases bedside workload and costs. For decades, unfractionated heparin (UFH) represented the standard CRRT anticoagulant. Drawbacks of UFH anticoagulation were the need for a high blood flow and an increased bleeding risk, particularly in surgical patients. In the early 90s, CRRT anticoagulation was revolutionized by the introduction of regional citrate anticoagulation (RCA) [13, 14]. Compared to UFH, RCA significantly decreased bleeding risk and prolonged circuit and FLS. The development of novel citrate formulations and diluted citrate solutions [15] further propagated RCA as a primary anticoagulant strategy in the intensive care unit. Guidance for optimal CRRT anticoagulation has been bundled in clinical algorithms [16], an example of which is depicted in Figure 2. However, according to the KDIGO guidelines, RCA is the first choice for CRRT anticoagulation, regardless of whether the patient is at risk for bleeding or not [6].
Prescribing RCA
A citrate concentration of 3–5 mmol/L should be attained before the filter to reach a post-filter ionised calcium level of 0.25–0.35 mmol/L (0.8–1.3 mg/dL) [15]. This is imperative to avoid coagulation inside the filter and the circuit. Correct prescription of citrate in any protocol requires, among others, dose adjustment to blood flow. Citrate is infused either separately or added to the replacement fluid. In the latter, currently most popular option, a fixed relation between citrate flow and blood flow is not guaranteed, as the flow of the replacement fluid varies with the ultrafiltration (UF) flow and the amount of removed fluid. For instance, when UF flow decreases or when a more negative fluid balance is desired, less citrate is administered and this may precipitate early filter clotting resulting in lower filter survival time. Adding citrate to the predilution fluid can overcome this problem.
Commercial citrate formulations contain tri-sodium citrate concentrations varying from 0.5 to 30%. The lower the concentration, the higher the volume infused (and thus the need for more storage space!) but also the lower the risk of citrate-related side-effects. Solutions also contain variable proportions of citric acid. Eventually, a citrate dextrose-A solution is used, which contains a fourfold higher citrate concentration than the 0.5% solutions (74.8 vs. 18 mmol/L) [15]. Equimolar citrate solutions may differ in sodium amount and buffer potential. For citrate dosing, a fixed blood flow/citrate flow relation is preferred, obviating the need for routine monitoring of anticoagulation in the extracorporeal circuit. If blood flow is kept constant and citrate dose adjusted to blood flow, metabolic control is recommended