Management for Electrolytes Disturbances during Continuous Renal Replacement Therapy

Abstract

Despite the lack of proven superiority in mortality compared to intermittent hemodialysis, continuous renal replacement therapy (CRRT) is the preferred renal replacement therapy modality for critically ill patients with acute kidney injury (AKI) due to better hemodynamic stability and steady correction of electrolytes disturbances and volume overload. Multiple and complex electrolyte disorders in patients with AKI can be managed effectively with CRRT because controlled and predictable correction is feasible. Thus, CRRT has an advantage with safety over conventional hemodialysis, especially in patients with both renal dysfunction and electrolyte disorder that require a sophisticated treatment with avoidance of rapid correction. On the contrary, CRRT can potentially lead to paradoxical disturbance of electrolytes such as hypokalemia or hypophosphatemia, especially in patients under high dose or prolonged duration of CRRT treatment. These electrolytes related complications can be prevented with close monitoring followed by the appropriate use of CRRT fluids. Although there is a lack of solid evidence and standardized guideline for CRRT prescriptions, optimal management of various electrolyte disturbances can be achieved with individualized and tailored dialysate and replacement fluid prescriptions. Several commercially available CRRT solutions with varying compositions provide flexibility to manage electrolyte disorders and maintain the stability of electrolyte. In this review, we discuss various prescription methods to manage common electrolyte imbalances as well as preventative strategies to maintain electrolyte homeostasis during CRRT providing detailed protocols used in our center. This review may contribute to future research that can lead to the development of clinical practice guidelines.

INTRODUCTION

Continuous renal replacement therapy (CRRT) is often used in critically ill patients with acute kidney injury (AKI)1,2). Although previous studies failed to show the survival benefits of CRRT over conventional intermittent hemodialysis, CRRT is the preferred renal replacement therapy (RRT) in critically ill patients with renal failure since it allows better hemodynamic stability and continuous treatment with excellent efficacy3). Moreover, steady acid-base and electrolyte correction are known additional advantages of CRRT compared with intermittent hemodialysis4,5).

Electrolyte disturbances are common in critically ill patients, and the incidence of complex electrolyte abnormality was found to be as high as 67%6). Many types of electrolyte disturbance can be effectively managed with CRRT with a continuous uninterrupted fashion7). Moreover, CRRT can provide additional benefits to patients with several types of electrolyte disturbances such as severe hypernatremia or hyponatremia because CRRT can reduce the risk of rapid- or over-correction8). However, paradoxically, CRRT treatment can result in electrolyte complications, including hypophosphatemia, hypokalemia, and hypomagnesemia, especially in patients under prolonged duration or high dose of CRRT5,9). In order to treat electrolyte disturbance with CRRT and to minimize CRRT-induced paradoxical electrolyte disturbances in critically ill patients, the application and prescription of dialysate and replacement fluid should be tailored and individualized according to clinical situations10).

In this review, we discuss clinical strategies to treat various types of electrolyte disturbances and avoid CRRT-induced electrolyte-associated complications.

Dysnatremia

Hypernatremia

Hypernatremia is a common complication in critically ill patients with AKI, occurring in 10% to 26% of patients11). In-hospital hypernatremia may be induced using diuretics or administration of hypertonic saline, and gastrointestinal loss11,12). Hypernatremia is associated with longer hospital stays and a greater risk of mortality compared with normonatremia13). Lowering sodium concentration induces the alteration of extracellular tonicity, leading to cellular swelling14). Generally recommended correction rate of serum sodium is ≤10 mmol/L over 24 h in patients with chronic hypernatremia12,15). However, unlike the strategy to treat hyponatremia, there is a lack of solid evidence that supports the need for slow correction in hypernatremia. Nevertheless, in hypernatremic patients who require RRT, it is important to note that concomitant dialytic removal of urea and uremic solutes may worsen brain edema and cause dialysis disequilibrium syndrome16). Thus, despite the controversy regarding the suggested correction rate for hypernatremia17), hypernatremia should be carefully managed with slow correction rate in patients under RRT. In general, CRRT allows a slower sodium concentration change compared to intermittent hemodialysis18), thus CRRT can be the best RRT modality in patients with severe chronic hypernatremia with renal failure.

In patients with severe hypernatremia who will undergo CRRT treatment, the correction rate can be managed by either hypertonic CRRT solutions or separate hypertonic saline infusions19). Given the lack of commercially available hypertonic CRRT fluids (Table 1), either sodium chloride or sodium bicarbonate can be added to the standard CRRT solutions to increase the sodium concentration to the desired level18,19). Sodium chloride can be mixed when patients have only hypernatremia without significant metabolic acidosis. When patients have both hypernatremia and metabolic acidosis, sodium bicarbonate can be considered as an initial choice. When continuous veno-venous hemodiafiltration (CVVHDF) mode is used, this method needs to be applied to both dialysates and replacement fluids15,20). Example concentrations after adding different amounts of sodium are presented in Table 2. The recommended sodium concentration for the initial CRRT solution is set to be 5-10 mmol/L lower than that of the patient15,20). Serial changes in serum sodium concentration should be frequently monitored. If the sodium concentration decreases by 2 or more within the first 6 hours after CRRT initiation, we recommend adjustment of the CRRT dose or sodium concentration of the CRRT solution21).

Table 1. Compositions of commercially available CRRT solutions in Korea.

^*Availability and trade names of the solutions may differ according to countries.

Table 2. Changes in the sodium concentration of a standard 5 L CRRT fluid (Na 140 mmol/L) after adding different amounts of extra sodium.

^*Sodium can be added as a sodium-chloride or sodium-bicarbonate

Administration of 3% saline intravenously with a separate intravenous access or into the return line of CRRT blood circuit can also be used as an alternative strategy to prevent rapid correction of hypernatremia18,19). When this method is applied, 3% saline should be discontinued when CRRT delivery is interrupted or discontinued to avoid exacerbating hypernatremia19).

If patients have suspected or proven to have increased intracranial pressure and require CRRT treatment, therapeutic hypernatremia as an osmotherapy can be induced or maintained by using hypertonic CRRT fluid as mentioned above22). For this purpose, the recommended serum sodium concentration has been suggested as 150-155 mmol/L22,23).

Hyponatremia

In patients with renal failure and severe hyponatremia, the initiation of CRRT can potentially result in a rapid correction of hyponatremia that increases the risk of osmotic demyelination syndrome24). The lower the initial sodium concentration, the higher risk of overcorrection25). If sodium concentration decreases by 2 or more within the first 6 hours after CRRT initiation, lowering the CRRT dose or sodium concentration of CRRT solution should be considered21,26). Since there is a lack of commercially available hypotonic CRRT solutions (Table 1), there are two available strategies to prevent a rapid correction of hyponatremia: dilution of CRRT fluid; and concomitant intravenous infusion of 5 or 10% dextrose water solution.

The dilution of CRRT fluid can be achieved by either adding various volumes of sterile water or by exchanging equal volumes of the CRRT fluid with sterile water to achieve a desired sodium concentration19,26,27,28,29). When CVVHDF mode is used, this dilution method needs to be applied to both dialysates and replacement fluids29). For continuous venovenous hemofiltration (CVVHF) and CVVHDF, diluted fluid may be used as pre- or/and post-filter replacement fluid26). Sodium concentration of post-filter replacement fluid exerts a slightly stronger impact on plasma serum sodium concentration compared to sodium concentration of pre-filter replacement fluid30). When the same CRRT fluids with supraphysiologic sodium concentration are used as both pre-filter and post-filter replacement fluids, the expected sodium correction rate will increase as the proportion of post-filter replacement flow rate increases compared to pre-filter replacement flow rate30). The calculated final concentrations following adding or exchanging different volumes of sterile water are presented in Table 3. However, the following caveats should be considered when this method is applied. The former method has a volume limitation that will fit in the manufacturer’s bag and can cause the CRRT machine’s scale alarm when a large volume is added. The latter method requires an additional volume removal process from CRRT fluid bag before adding distilled water and increases the risk of contamination27).

Table 3. Changes in the sodium concentration of a standard 5 L CRRT fluid (Na 140 mmol/L) after adding or exchanging sterile water.

A concomitant intravenous infusion of dextrose water solution into a separate intravenous access or return bloodline of the CRRT circuit can be an alternative strategy to reduce the sodium correction rate8). Our center has used an infusion of 5% dextrose water solution with a separate intravenous access starting with the rate of 1.5 mL/kg/h with serum electrolyte follow-up every 4 hr. Although this method is less cumbersome compared to diluting CRRT fluid, a large volume of 5% dextrose water infusion with high rate (more than 200 cc/h) is frequently inevitable to prevent rapid correction in hyponatremic patients prescribed with a high dose of CRRT treatment due to other metabolic derangements.

Dyskalemia

Hyperkalemia

Potassium homeostasis is primarily controlled by renal excretion. Potassium is an essential element for maintaining cellular function. An abnormal serum potassium concentration can cause deleterious consequences such as cardiac arrhythmia and sudden cardiac death. Hyperkalemia is a major complication of AKI, which occur in 8.8-32.2%31). Adrenal insufficiency and medications such as angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and potassium-sparing diuretics can contribute to the development of hyperkalemia32). A U-shaped association between baseline serum potassium and all-cause mortality was reported in critically ill patients33,34). In patients requiring CRRT, mortality significantly increased when pre-CRRT potassium level ≤3.4 mmol/L or ≥4.5 mmol/L35).

Although CRRT can be used as a treatment for hyperkalemia, in patients with severe hyperkalemia with EKG changes, intermittent hemodialysis should be considered as a first-line RRT modality rather than CRRT since the removal rate of conventional hemodialysis is higher than that of CRRT36). Approximately 70-100 mmol of potassium can usually be removed during 4 hours of dialysis31,37). CRRT can also be used as a treatment for hyperkalemia when hemodialysis is not feasible18). CRRT can effectively correct hyperkalemia by increasing the dialysate or replacement flow rate and using low potassium or potassium-free CRRT fluids38). The potassium concentration of CRRT solutions ranges from 0 to 4 mmol/L (Table 1). In patients with life-threatening hyperkalemia, potassium-free solutions with a higher CRRT dose should be applied initially. Mild hyperkalemia can be corrected by using CRRT solutions with a potassium concentration of 2 mmol/L18,20,39). In patients with progressive tissue damage such as rhabdomyolysis, tumor lysis syndrome, or hemolysis, ongoing potassium load should be considered when choosing CRRT solutions based on their serum potassium concentrations35,39).

If hyperkalemia persists while the maintenance of appropriately prescribed CRRT, it should be considered that there can be an ongoing tissue breakdown such as rhabdomyolysis or hemolysis as well as hypercatabolic states such as severe sepsis or burn35,39). Particularly, in patients using extracorporeal membrane oxygenation or ventricular-assisted devices, hemolysis should be excluded35,39). Insufficient actual delivered dose than the prescribed dose possibly due to frequent interruptions of CRRT, decreased dialyzer efficiency, or recirculation of vascular access may also cause persistent or recurrent hyperkalemia35).

Hypokalemia

Hypokalemia is less frequent than hyperkalemia in critically ill patients with AKI35), but it occurs more frequently as a complication of CRRT with an incidence as high as 24%5,9). When a conventional dose (20-25 mL/kg/h) of CVVHDF with potassium-free dialysate and replacement fluids is prescribed, hypokalemia was reported to occur as early as the first 24 hours after CRRT initiation40). Since significant hypokalemia can induce respiratory muscle weakness and cardiac arrhythmias41,42), avoiding hypokalemia in critically ill patients is important. Moreover, given the fact that chronic potassium depletion can lead to renal tubular cell damage and dysfunction, hypokalemia should be avoided in AKI patients for better renal recovery43).

Hypokalemia during CRRT can be treated or prevented with oral/intravenous potassium supplementation and/or using potassium-containing CRRT solutions18). Compared to potassium-free CRRT solutions, patients treated with potassium-enriched CRRT solutions showed significantly higher serum potassium concentration during CRRT40). Using potassium-containing CRRT solutions can reduce the intensive care unit (ICU) workloads and frequency of intravenous supplementation44).

Thus far, there is a lack of consensus on recommended potassium concentration in CRRT fluids. Many centers use protocols to prescribe CRRT dialysate based on serum potassium and phosphate level. An example of a CRRT fluid prescription algorithm based on patients’ potassium concentration is presented in Table 4. We use CRRT solutions with a potassium concentration of 4 mmol/L as dialysate fluid and pre-filter replacement fluid when the patient’s serum potassium is ≤4.5 mmol/L. When serum potassium concentration is 4.5-5.0 mmol/L, solutions with a potassium concentration of 2 or 4 mmol/L were used. When serum potassium >5 mmol/L, solutions with a potassium concentration of 0 mmol/L were used. Most centers do not use a potassium concentration 4 mmol/L solutions for post-filter replacement fluid to avoid potential risk of hyperkalemia. Potassium concentrations should be monitored every 4 to 8 hours depending on the patients’ condition20,44).

Table 4. An example of CRRT fluid protocol according to serum potassium and phosphate concentrations using commercially available phosphate and potassium-containing CRRT fluids.

^*Post-filter replacement fluid is fixed with Hemosol B0

^†This protocol is based on the application of the same flow rate for dialysate and replacement fluid (The used ratio for pre- and post-filter replacement fluid flow rates ranged from 1:1 to 4:1).

Dyscalcemia

Hypercalcemia

Calcium is associated with cellular injury and is known to be an important factor in maintaining cellular function45,46). Hypercalcemia induces vasoconstriction which reduces the glomerular filtration rate, and decreases renal reabsorption of water in kidneys, leading to volume depletion47). Hypercalcemia can aggravate AKI by promoting renal tubular injury48). Hypercalcemia can occasionally occur in AKI patients with malignancy or immobilization or in those taking vitamin D-containing drugs47,49,50,51).

In patients with severe hypercalcemia, aggressive fluid resuscitation with normal saline is required to restore intravascular volume. RRT need to be considered for patients who are unsuitable for aggressive fluid therapy due to volume overload or refractory to medications such as intravenous bisphosphonate and calcitonin51). The ionized calcium concentration of the commercial CRRT solutions is about 1.25-1.75 mmol/L (2.5-3.5 mEq/L) (Table 1), thus calcium balance during CRRT is neutral or mildly positive18,39).

When performing CRRT in AKI patients with significant hypercalcemia, calcium-free solutions can be used as dialysate and replacement fluid. In general, CRRT solutions usually consist of two separate chambers, one (compartment A) containing sodium bicarbonate and sodium chloride and the other (compartment B) containing calcium chloride and magnesium chloride. This system is designed to prevent precipitations of bicarbonate with calcium and magnesium by reconstituting two compartments immediately before its use18). In patients with significant hypercalcemia, only the calcium-free chamber (compartment A) can be utilized without the reconstitution of the two compartments. We use this strategy in patients with serum ionized calcium concentration ≥1.4 mmol/L. By applying this method for replacement fluid, our center lowered hypercalcemia incidence during CRRT. However, this method can potentially induce hypomagnesemia since calcium containing compartment B contains magnesium as well. Therefore, frequent monitoring of serum calcium and magnesium concentration is mandatory to avoid hypocalcemia and hypomagnesemia20). An example of a detailed algorithm for patients with hypercalcemia in conjunction with serum potassium and phosphate concentrations is presented in Table 5.

Table 5. An example of CRRT fluid protocol for patients with significant hypercalcemia.

^*Frequent monitoring of serum magnesium is required to avoid hypomagnesemia.

^†This protocol is based on the application of the same flow rate for dialysate and replacement fluid (The used ratio for pre- and post-filter replacement fluid flow rates ranged from 1:1 to 4:1).

CRRT with regional citrate anticoagulation (RCA) can also be used for the treatment of hypercalcemia. Several case series have been reported successfully treated hypercalcemic crises using RCA-CRRT with a low rate of calcium replacement52,53).

Hypocalcemia

Hypocalcemia is commonly encountered in the ICU and known to be a predictor of increased mortality in critically ill patients with AKI. The mortality rate of critically ill patients with hypocalcemia was found to be as high as 50%54,55,56). Serum calcium concentration was inversely correlated with the severity of AKI with the lowest in the patients with uremic encephalopathy57). Hyperphosphatemia, parathyroid hormone (PTH) insufficiency, decreased production of renal calcitriol, sepsis, and various medications can cause hypocalcemia in critically ill patients58).

In RCA-based CRRT, citrate is infused into the pre-filter bloodline, and the citrate chelates ionized calcium. Therefore, RCA-based CRRT has a higher incidence of hypocalcemia than heparin-based CRRT. To prevent hypocalcemia during RCA-based CRRT, calculating the rate of calcium loss and administrating intravenous calcium is needed to maintain. The infusion rate of calcium supplementation should be adjusted according to the serial changes in serum ionized calcium concentration59,60). Ionized calcium levels from pre-filter and post-filter sites should be monitored every 6-8 hours61). One center’s protocol suggested starting 5% calcium chloride infusion at 5.5 mmol/h (25 ml/h) and increasing the rate by 2 ml/h when systemic ionized calcium concentration ranges from 0.8 to 1.0 mmol/L. The rate of calcium infusion can be reduced by 2 ml/h if systemic ionized calcium ranges from 1.2 to 1.4 mmol/L62). Additionally, it is important to note that total calcium concentration should be monitored at least once daily to calculate the calcium gap or ratio. Since an assay to directly measure calcium-citrate complex is currently unavailable, increasing a gap between total calcium and ionized calcium or total/ionized calcium ratio can be used as an indicator of citrate accumulation63,64). In the case of citrate accumulation, the available management includes reducing/stopping the citrate infusion, decreasing blood flow rate to decrease blood-citrate coupling, increasing dialysate and/or filtration rate to enhance citrate clearance, and increasing calcium infusion to avoid or treat ionized hypocalcemia63,64).

Evidence for adequate calcium replacement such as threshold and the appropriate dose is lacking65). To normalize serum ionized calcium levels in hypocalcemic patients under CRRT, calcium gluconate or calcium chloride can be injected by bolus or continuous infusion66). Several studies have reported that ionized calcium concentration increases immediately after calcium administration but is not maintained until after 3 to 6 hours67). Further study regarding calcium supplementation strategies such as threshold, appropriate dose, timing, and duration in AKI patients undergoing CRRT is required65).

Dysphosphatemia

Hyperphosphatemia

Phosphate is an intracellular anion and essential for cellular biologic function68). Serum phosphate concentration is determined by the renal excretion capacity of dietary phosphate intake. Although phosphate balance can be maintained by increased PTH and fibroblast growth factor 23 by decreasing proximal tubular reabsorption, urinary excretion cannot reach adequate phosphate excretion once GFR decline below 20-25 mL/min. Hyperphosphatemia was reported to be associated with adverse patient outcome69,70), but it is unclear whether hyperphosphatemia has direct toxicity like other electrolytes, or it simply reflects severity of underlying catabolic conditions. However, acute severe hyperphosphatemia in catabolic conditions may contribute to organ dysfunction by inducing hypocalcemia and precipitating calcium phosphate crystals71) In these conditions, calcium supplementation and correction of metabolic acidosis can further promote calcium phosphate crystal formation. Therefore, severe hyperphosphatemia-induced symptomatic hypocalcemia should be considered as an indication of RRT, especially in patients with excess tissue breakdown such as tumor lysis syndrome72). Hyperphospha-temia can be easily managed by CRRT treatment since phosphate is readily removed by diffusion and convection9), but the evidence supporting the beneficial effect of treating hyperphosphatemia in AKI is lacking.

Hypophosphatemia

Since phosphate concentration of most CRRT solutions is 0 mmol/L (Table 1), the incidence of hypophosphatemia was reported as high as 65% while using these non-phosphate-containing CRRT solutions5,9). Thus, hypophosphatemia is considered as one of the most serious complications in patients who underwent CRRT. Hypophosphatemia is associated with respiratory muscle weakness, and myocardial dysfunction, arrhythmia, leukocyte dysfunction, rhabdomyolysis, and increased mortality73,74). Given that phosphate depletion is associated with impaired phagocytosis leading to immune dysfunction75,76), avoiding hypophosphatemia is a critical issue in critically ill patients. Notably, in a study that applied the protocol-driven phosphate repletion with a sophisticated calculation of urinary and CRRT-derived phosphate loss, the net phosphate balance remained constantly negative77). Although negative phosphate balance is usually necessary during early period of CRRT in AKI patients due to hyperphosphatemia caused by reduced renal phosphate excretion, persistent negative phosphate balance exerts a potentially harmful effect particularly in patients under a prolonged course of CRRT treatment. Furthermore, catecholamine administration, which is frequently required in patients under CRRT, can result in intracellular shifting of phosphate, which further contributes to CRRT-associated hypophosphatemia78).

As a preventative intervention, oral or intravenous phosphate replacement can be applied, or phosphate can be added to CRRT solutions. For example, 15 mmol sodium phosphate can be intravenously injected over 4 hours twice to 3 times per day during CRRT treatment. Although there was a concern about adding phosphate to CRRT solution due to the potential risk of calcium phosphate precipitation, it has been studied that potassium phosphate can be added to calcium-containing CRRT solution without calcium phosphate precipitation up to 2 days nor adverse events in patients under CRRT79). A study that sophisticatedly measured ionized calcium and phosphate concentrations in the solution bag after adding potassium phosphate found no change in either of them for up to 5 hours80). Therefore, adding potassium phosphate to CRRT solution right before its application to the patient is likely a safe strategy in centers where commercialized phosphate-containing CRRT solutions are not available.

The commercialized phosphate-containing CRRT solution was approved by US Food and Drug Administration in 2015. Since then, many centers have adopted phosphate-containing solutions with potential advantages in avoiding medical error and contamination81,82). Our center uses premixed phosphate-containing CRRT solution with a phosphate concentration of 1.2 mmol/L (3.7 mg/dL) as a dialysate fluid and pre-filter replacement fluid when patients’ serum phosphate level is ≤3.5 mg/dL before initiation of CRRT treatment or during the treatment20). More specifically, considering that phosphate-containing CRRT solutions have high potassium concentration (4.0 mmol/L) (Table 1), we apply phosphate-containing solution as both dialysate and pre-filter replacement fluid in patients with serum potassium <4.5 mmol/L and serum phosphate <3.5 mg/dL (Table 4). In patients with a serum potassium concentration of ≥4.6 and ≤5.0, we apply it as a dialysate only (Table 4). After using this protocolized application of phosphate-containing CRRT solution, the variability of the serum phosphate concentration during CRRT treatment was significantly reduced in our center20).

A recent retrospective single-center study demonstrated that the use of non-phosphate solution has 8-fold higher risk of hypophosphatemia compared to the phosphate-containing solution82). Furthermore, patients who received phosphate-containing CRRT solution showed shorter hospital stays and longer ventilator-free days83).

Dysmagnesemia

Hypermagnesemia

Magnesium is a physiologically important electrolyte involved in muscle contraction and relaxation as well as neurotransmission84). Hypermagnesemia can occur in patients with impaired renal function and increased intake of magnesium because renal excretion is the only route of magnesium elimination85). In line with the experimental studies showing that magnesium mediates vasorelaxation86), epidemiologic studies demonstrated an association between hypermagnesemia and lower blood pressure as well as increased vasopressor requirements87). Particularly, hypermagnesemia can cause vasoactive drug refractory hypotension with cardiac depression88). If medical treatments including aggressive intravenous saline administration and loop diuretics fail to effectively reduce magnesium concentration in symptomatic severe hypermagnesemic patients, hemodialysis or CRRT should be considered to remove excess magnesium. Given that severe hypermagnesemia frequently occurs in the setting of increased magnesium absorption due to impaired bowel motility and hypermagnesemia per se can further aggravate ileus with the interference of smooth muscle extraction and contraction coupling89), it is important to note that continuous absorption may exist in hypermagnesemic patients even after discontinuation of magnesium intake or administration. As such, CRRT can be a suitable treatment option for hypermagnesemic patients because its continuity by preventing rebound hypermagnesemia90).

Hypomagenesemia

Hypomagnesemia can derive Na-K-ATPase dysfunction altering cardiac repolarization, which can contribute to cardiac arrhythmia in critically ill patients91). Hypomagnesemia can also result in respiratory muscle weakness in critically ill patients92). Commercial CRRT fluids have 0.5-0.75 mmol/L (1-1.5 mEq/L) of magnesium(Table 1). Especially in the setting of RCA, hypomagnesemia can happen more frequently because magnesium is chelated by citrate, and magnesium-citrate complexes have high diffusive and convective clearance93).

There is a lack of recommendations for magnesium supplementation in patients undergoing CRRT. If hypomagnesemia occurs in patients under CRRT, intravenous magnesium can be administered94). A widely available intravenous magnesium formulation is magnesium sulphate (MgSO₄), where 1 g of MgSO₄ contains 100 mg, corresponding to 4 mmol (8 mEq) of elemental Mg²⁺95). MgSO₄ 1 g can increase serum magnesium concentration by 0.18 mg/dL within 18-30 hours. It is important to note that intravenous magnesium supplementation can cause arrythmia, hypotension, and neuromuscular depression96). In RCA protocols, a continuous infusion of 2-4 g/day of MgSO₄ is generally administered.

SUMMARY and CONCLUSIONS

Multiple and complex electrolyte disturbances are common in critically ill patients with AKI, and many of them can be effectively managed by CRRT. Furthermore, for the electrolyte imbalances that require slow correction such as dysnatremia, CRRT has the advantage compared to conventional intermittent hemodialysis. However, unintended electrolyte complications may occur during CRRT, especially with prolonged duration and high intensity of treatment. Close monitoring of electrolytes accompanied by tailored prescriptions of CRRT solutions, intravenous fluids, and supplementary medications are required in CRRT treatment. Recently, several centers introduced protocol-driven CRRT prescription strategies, showing improved electrolyte stability and reduced labor-intensive repetitive electrolyte replacement and medical costs. We believe that a sophisticated algorithm-based approach in CRRT management can improve patients’ outcomes and prevent treatment-related adverse effects. Thus far, there is a lack of consensus regarding electrolyte management among CRRT. The development of a systemized operation protocol by prospective clinical trials is warranted to improve the outcomes of patients and augment the advantages of CRRT treatment.