A 54-year-old male presents with septic shock requiring vasopressor support and continuous renal replacement therapy for acute kidney injury (AKI).

His blood tests on presentation show:

Parameter

Patient Value

Adult Normal Range

FiO2

0.4

pH

7.15*

7.35 – 7.45

pO2

146.0 mmHg (19.5 kPa)

pCO2

42.0 mmHg (5.6 kPa)

35.0 – 45.0 (4.6 – 6.0)

SpO2

98%

Bicarbonate

14.0 mmol/L*

22.0 – 26.0

Base Excess

-13.6 mmol/L*

-2.0 – +2.0

Lactate

1.4 mmol/L

0.5 – 1.6

Sodium

104 mmol/L*

135 – 145

Potassium

4.0 mmol/L

3.5 – 5.0

Chloride

73 mmol/L*

95 – 105

Glucose

4.1 mmol/L

3.5 – 6.0

Urea

35.6 mmol/L*

3.0 – 8.0

Creatinine

947 µmol/L*

45 – 90

Albumin

28 g/L*

35 – 50

  1. With regards to his electrolytes, what is the concern about performing renal replacement therapy on this patient?                                                                   (10% marks)
  1. List three ways by which you could reduce this risk.                                          (40% marks)

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College answer

  • a)

    Patient is hyponatraemic (duration unknown) -concern about rapid correction of Na causing osmotic demyelination syndrome (although uraemia may be protective) – should be aiming for 6-8 mmol/24 hrs which may be problematic if using standard bags (with normal Na levels) for CRRT as correction may occur more rapidly

    b)

  • CRRT at lower doses than usual i.e. very low flow rate to try to minimise speed of electrolyte correction and for short intervals only.
  • Add sterile water to dialysis or replacement fluid so that solution patient is being dialysed against has a lower sodium than standard solution (e.g. dilute to Na 117mmol/L or less – formulas exist to determine amount of sterile water to be added – candidates were not expected to know values/calculations)
  • Give the patient additional free water/5% dextrose intravenously while receiving CRRT (and remove this volume on circuit)

Examiners Comments:

 Part c - a lot of candidates focussed on the urea and potential disequilibrium syndrome rather than the far more concerning hypoatraemia and potential OSM.

Discussion

Interestingly, this ABG question did not specifically require the trainee to interpret the findings, which made it a time-wasting honeypot for people who did not read the question properly.

There is really not much to add to the college answer here. In essence, the standard dialysate which contains 145 mmol/L will correct this patient's sodium way too quickly. In fact, according to Bender et al (1998) standard IHD dialysis can raise the sodium by 5mmol/L per every hour of a 4-hour session. Obviously that's not ideal, and some strategies are required to keep the patient from developing osmotic demyelination.

Of all the possible resources to answer this question, the article by Rosner & Connor (2018) is so good that one might think one of the examiners has a subscription to th Clinical Journal of the American Society of Nephrology.  In short, the possible methods of mitigating the risk of myelinolysis in a hyponatremic dialysis patient are:

  • Avoid dialysis altogether. Sure, the patient is acidotic, but one could surely use some THAM to correct that, and there's no mention of fluid overload in the stem. 
  • Give sodium, then dialyse. If the patient needs dialysis but still passes some urine and is otherwise asymptomatic, one can spare 48-72 hours to bring the sodium up to a level where demyelination will not be such a massive risk (eg. 125mmol/L or so) and then carry on with dialysis as usual.
  • Use low dose dialysis. The dialysate flow rate can be turned down to the point where electrolyte exchange across the membrane is slow and gentle. The downside of this would be slower solute clearance, potentially so slow that it has no clinical benefit. As sodium ions are more likely to exchange across the membrane than the relatively larger urea molecules, one may find oneself in a position were no useful metabolic waste clearance has taken place, but the patient's sodium has corrected dangerously quickly anyway. Even if this dangerous outcome does not occur, one could still advance the logical argument that having pointless dialysis has zero advantage over having no dialysis.
  • Give systemic 5% dextrose. The patient will gain sodium via the circuit, so you give them water at the same time. This works just fine, so long as you keep giving enough 5% dextrose to keep up with the sodium exchange rate. With the dialysate flow low enough and the dextrose rate high enough, you should be able to achieve any desired rate of rise of sodium. Of course, this is not without its disadvantages. For one, that's 66 mmol/L of dextrose you're giving, which will have an undesirable effect on their BSL. Secondly, that's potentially several litres of extra fluid you are giving, which can't possibly be benign for this patient's circulatory system. Obviously at some later stage you will have to take that water out via the circuit, as the renally incompetent patient is probably not up to excreting it themselves. And when you take it out with the circuit, the sodium will go up again.  
  • Give sterile water or 5% dextrose into the return line of the circuit. That's functionally the same step as above, but one less access line.
  • Alter the sodium content of the dialysate. This takes some people out of their comfort zone, as one needs to create one's own bags of sterile dialysate. To quote the case report by Bender et al (1998)"Each 2 liters of dialysate was prepared by mixing 1 liter of 5% dextrose and 0.45% NaCl (half normal saline) with 1 liter of 0.675% NaCl (three-quarters normal saline) to which 50 mEq NaHCO3 was added; the final sodium concentration was thus 121 mEq/L"

References

References

Zepeda-Orozco, Diana, and Raymond Quigley. "Dialysis disequilibrium syndrome." Pediatric nephrology 27.12 (2012): 2205-2211.

Arieff, Allen I., et al. "Brain water and electrolyte metabolism in uremia: effects of slow and rapid hemodialysis." Kidney international 4.3 (1973): 177-187.

Bender, Filitsa H. "Successful treatment of severe hyponatremia in a patient with renal failure using continuous venovenous hemodialysis." American journal of kidney diseases 32.5 (1998): 829-831.

Wendland, Erik M., and Andre A. Kaplan. "A Proposed Approach to the Dialysis Prescription in Severely Hyponatremic Patients with End‐Stage Renal Disease." Seminars in dialysis. Vol. 25. No. 1. Oxford, UK: Blackwell Publishing Ltd, 2012.

Rosner, Mitchell H., and Michael J. Connor. "Management of severe hyponatremia with continuous renal replacement therapies." Clinical Journal of the American Society of Nephrology 13.5 (2018): 787-789.