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 |
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)
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.
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:
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.