40 Years of Continuous Renal Replacement Therapy. Группа авторов

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      –Metabolic alterations: metabolic acidosis, increased anion gap, decreased ionized calcium, rising calcium ratio and calcium gap, increased lactate.

–Therapy: reduce or stop citrate, continue CVVH without anticoagulation or under low dose heparin, supply calcium (target a ionized calcium of 1.0 mmol/L [between 4 and 5 mg/dL] [15, 23]).

      Citrate Intoxication?

      –Cause: accidental over-infusion of citrate or decrease of UF flow below the lower limit at constant citrate infusion rate.

      –Metabolic alterations: metabolic alkalosis, low ionized calcium, and proportional rise of calcium ratio as a result of alkalosis.

      –Treatment: withdraw citrate infusion.

      Hypocalcemia?

      –Cause: citrate accumulation.

      –Therapy: calcium infusion. Since most critically ill patients have some degree of hypocalcemia, the targeted ionized calcium level should be approximately 1.0 mmol/L (4 mg/dL).

      Metabolic Alkalosis?

      –Cause: excessive bicarbonate substitution relative to UF flow.

–Treatment: substitution of more buffer-free and less bicarbonate-buffered solution. The use of normal saline (400–800 mL/h) instead of bicarbonate, as substitution liquid was recently shown to effectively correct metabolic alkalosis [24].

      –Specific situations:

      a. Declining UF flow while citrate infusion remains fixed adjusted to blood flow. Treatment: filter change if UF flow is less than 1,500–2,000 mL/h (depending on blood and citrate flow).

      b. Metabolic conversion of accumulated citrate with recovering liver function. Treatment: replacement with buffer-free solution or halving citrate dose in pre-dilution.

      c. Accidental over-infusion of citrate. Treatment: withdraw citrate infusion, replacement with buffer-free solution, increase UF flow as needed.

      Hypomagnesemia?

      –Cause: increased loss of citrate-bound magnesium by ultrafiltration.

–Treatment: infusion of magnesium together with calcium. Magnesium levels must be maintained between 2 and 4 mmol/dL [15, 25].

      Hypokalemia?

      Potassium levels must be kept strictly between 4 and 5 meq/dL.

      Steadily Increasing Calcium Infusion Rate?

      Care must be taken when calcium infusion rate augments every 2–4 h, even when transient or in the presence of concomitant hypocalcemia or hypomagnesemia.

      When going beyond 0.8 mg/dL over 4–6 h, citrate accumulation must always be considered.

      Hypernatremia?

      –Cause: high citrate flow relative to UF flow. May occur when UF flow gradually declines at unchanged citrate flow. Metabolic alkalosis is mostly present.

      –Treatment: filter change if TMP >250 mm Hg, target normal sodium concentration, buffer-free solution.

      Hyponatremia?

      –Cause: use of substitution solutions with low sodium content. Since such solutions contain no buffer, metabolic acidosis may arise.

      –Treatment: substitution with normal saline, bicarbonate-buffered solution.

      Monitoring of Metabolic Variables and Coagulation Efficacy?

      –At 4-h interval: measurement of Na⁺, K⁺, Cl⁻, ionized calcium, blood gas, (strong) anion gap calculation,

      –Once daily: total calcium (to calculate calcium ratio or calcium gap), magnesium,

      –Once or twice daily: creatinine, urea, phosphate,

      –Monitoring intervals can be progressively prolonged in stable patients,

      –Monitoring efficacy of circuit anticoagulation is necessary at the start of treatment and may be continued at the physician’s discretion thereafter. A post-filter ionized calcium level of 0.25–0.35 mmol/L (0.8–1.3 mg/dL) is targeted.

      Conclusions

      Vascular access and anticoagulation for CRRT have considerably evolved over the years. Dialysis catheters are preferentially placed in the RIJ vein with the tip positioned in the right atrium. Ultrasound guidance may assist in placing the catheter. Femoral vein catheterization is a valuable alternative. Future improvements in catheter “technology” and performance are awaited, in particular for use in combined extracorporeal techniques (e.g., low flow extracorporeal CO₂ removal embedded in a CRRT circuit).

      RCA has revolutionized anticoagulation by allowing lower circuit blood flow, causing less bleeding accidents, and creating better filter performance. However, implementing RCA requires careful monitoring, including early detection and anticipation of potential citrate-related metabolic complications. Novel citrate solutions are being developed that will allow more optimal metabolic fine-tuning.

      References

1Honore PM (Editor-in-Chief): Renal replacement in critical care; in Honore PM, Joannes-Olivier O, Spapen HD, Bihorac A (eds): Textbook 269 pages. Lambert Academic Publishing release in February, 2016.

      2Glazer S, Saint L, Shenoy S: How to prolong the patency of vascular access. Contrib Nephrol 2015;184:143–152.

3Granata A, D’Intini V, Bellomo R, Ronco C: Vascular access for acute extracorporeal renal replacement therapies. Contrib Nephrol 2004;142:159–177.

4Parienti JJ, Mégarbane B, Fischer MO, Lautrette A, Gazui N, Marin N, Hanouz JL, Ramakers M, Daubin C, Mira JP, Charbonneau P, du Cheyron D; Cathedia Study Group: Catheter dysfunction and dialysis performance according to vascular access among 736 critically ill adults requiring renal replacement therapy: a randomized controlled study. Crit Care Med 2010;34:1118–1125.

5Morgan D, Ho K, Murray C, Davies H, Louw J: A randomized trial of catheters of different lengths to achieve right atrium versus superior vena cava placement for continuous renal replacement therapy. Am J Kidney Dis 2012;60:272–279.

6Lameire N, Kellum JA; KDIGO AKI Guideline Work Group: Contrast-induced acute kidney injury and renal support for acute kidney injury: a KDIGO summary (part СКАЧАТЬ