Dialysis Solutions and Replacement Fluids

Sodium and Potassium

As opposed to intermittent HD or prolonged intermittent renal replacement therapy (PIRRT), in which modulation of dialysate sodium concentration may be required to avoid too rapid modifications of serum sodium concentration, CRRT solutions are generally available at a standard sodium concentration around 140 mmol/L. An exception is represented by the dialysate/replacement fluids used in combination with hypertonic in sodium, high-concentration citrate solutions for regional citrate anticoagulation (RCA); in this case, low-sodium concentration CRRT solutions are required to avoid the occurrence of hypernatremia (see Table 143.2 ).

On the other hand, although the rapidity of electrolyte derangements correction during CRRT could be handled by the modulation of CRRT dose and exchanged volumes, the sodium content in dialysate/replacement solutions is not easily adjustable in the case of patients with severe hypernatremia and AKI requiring CRRT. To minimize the potential risk for a rapid decline in serum sodium levels, a sodium kinetic equation recently has been proposed to guide sodium concentration adjustments aimed at customizing CRRT solutions according to baseline serum sodium concentration; the kinetic model was also able to estimate the expected serum sodium levels throughout continuous venovenous hemofiltration (CVVH) days in relation to different sodium concentrations in the replacement fluid. However, to prevent errors and/or sterility breach, the same authors underlined the need of particular caution during solutions customization.

For CRRT use, dialysate/replacement fluids with a potassium concentration between 0 to 4 mmol/L are appropriate and commercially available (see Table 143.1 ). Using the more commonly adopted CRRT dose of 25 to 35 mL/kg/hr, most cases of hyperkalemia can be managed with potassium concentrations of 2 mmol/L. Lower potassium concentration solutions should be managed carefully to prevent hypokalemia and its related complications. In case of hypokalemia, the addition of potassium in dialysate/replacement fluids should be discouraged for safety reasons; if needed, protocol-guided separate infusion of potassium chloride appears to be safer and effective (see Table 143.2 ).

Buffer

Because the goal of RRT is the normalization of blood solutes concentration, the composition of RRT solutions should be targeted to obtain the more appropriate concentration gradient for the main solutes and to correct and/or prevent electrolyte and acid-base derangements in patients with renal failure. Metabolic acidosis represents a frequent acid-base derangement in patients with AKI, and severe metabolic acidosis is included among the indications for starting RRT. Therefore the buffer component of CRRT fluids requires special attention. The dialysis fluid should contain sufficient alkali to buffer metabolic acid production. Theoretical options for correction of metabolic acidosis in patients with AKI include acetate, lactate, bicarbonate, and citrate.

However, the use of acetate, largely abandoned also in end-stage renal disease (ESRD) patients in view of the associated hemodynamic instability, was never introduced in AKI patients undergoing CRRT. Original CRRT solutions contained lactate as the main buffer. Under normal conditions, lactate is metabolized rapidly, thereby generating an equimolar amount of bicarbonate and resulting in adequate correction of acidosis in most patients. However, in critically ill patients, lactate metabolism may be impaired and endogenous lactate production increased as a result of hypoxia, sepsis, or liver dysfunction. Thus, in patients with inadequate lactate metabolism, insufficient lactate conversion results in worsening acidosis, especially because bicarbonate losses are ongoing in the extracorporeal circuit (see Table 143.2 ). The risk of “lactate intolerance” is highest in patients with liver failure (impaired lactate clearance) or circulatory shock (increased endogenous lactate production). Therefore, in recent years, bicarbonate has gained popularity because of concerns that lactate may not be metabolized rapidly in the setting of multiple organ dysfunction syndrome (MODS), a frequent condition in ICU patients with AKI. Few adequately designed trials, along with several observational studies, have compared different buffers during RRT in AKI patients; most of them have been performed during CRRT and showed that the use of bicarbonate, compared with lactate, generally is associated to a better correction of acidosis, lower lactate levels, and improved hemodynamic tolerance, especially in AKI patients with circulatory shock.

On the basis of these findings, the 2012 KDIGO Guidelines on AKI suggest using bicarbonate, rather than lactate, as a buffer in dialysate and replacement fluid for RRT in patients with AKI, especially if associated with liver failure and/or lactic acidosis. The same guidelines recommend using bicarbonate rather than lactate as a buffer in dialysate and replacement fluid for RRT in patients with AKI and circulatory shock. Homemade bicarbonate solutions for CRRT largely have been abandoned for the higher risk of bacterial contamination and because of their instability when stored for prolonged periods. Indeed, bicarbonate solutions may form insoluble precipitates when combined with magnesium and calcium. In the last decade, this issue has been overcome by the worldwide introduction of commercially manufactured CRRT solution bags characterized by two separate chambers (bicarbonate and electrolytes) to be mixed bedside at the time of treatment start. When bicarbonate-containing dialysis fluid is used, the bicarbonate concentration should be sufficiently high to correct preexisting acidosis and to compensate for ongoing acid generation without inducing metabolic alkalosis. These goals generally can be achieved at a bicarbonate concentration of 32 to 35 mmol/L (see Table 143.1 ).

The use of citrate-buffered replacement solutions is discussed below.