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Abstract: PO1442

Neuroprotective Hypernatremia in Acute Liver Failure Using CRRT: A Challenging Scenario

Session Information

Category: Trainee Case Report

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Author

  • Cote, Jean Maxime, Centre Hospitalier de l'Universite de Montreal, Montreal, Canada
Introduction

Acute liver failure is associated with severe complications, including encephalopathy. Cerebral edema may occur, leading to increased intracranial pressure. Urgent medical management sometimes includes neuroprotective hyperosmolality and ammonia control using convective techniques. We describe a patient where high-volume CVVHDF was used to increase ammonia clearance while maintaining therapeutic hypernatremia.

Case Description

A 64-year-old female with severe bipolar disorder presented into the ED ~24hours after voluntary ingestion of ~150 tablets (75g) of acetaminophen. She was initially confused with normal blood pressure. Laboratory work showed severe metabolic acidosis with the following values: lactate 9.1 mmol/L, pH 6.99, ammonia 409 mmol/L, ALT 6398 U/L, creatinine 44 μmol/L, INR 9.1 and acetaminophen 250.2 mg/L. NAC and IV bicarbonate were quickly initiated, and a short plasmapheresis treatment was started 12hours later, inducing moderate hypercalcemia, hypernatremia (153 mmol/L) and normalising INR temporarily. Encephalopathy, oliguria and hemodynamic instability progressed. High-volume CVVHDF (90 mL/kg/h) was started at day 3 to optimise ammonia clearance and electrolytes. Hypertonic NaCl 23.4% (50 mmol) was added to a low-calcium 5L dialysate preparation (PrismOcal22) to obtain [Na] of 150 mmol/L. Over the next 3 days, additional hypertonic NaCl was required (until 80 mmol) (dialysate [Na] 156 mmol/L) to reach the ~150 mmol/L serum sodium targeted. However, after numerous medical complications, the patient was declared ineligible to liver transplantation and palliative care was initiated. She died 3 weeks after initial admission.

Discussion

Usage of high-volume CRRT in severe hepatic encephalopathy increases despite the paucity of evidence. Commercial standard solutions of dialysate used for CRRT usually have fixed sodium concentration (140 mmol/L). Adding sterile hypertonic NaCl into the dialysate bag allows us to modify its tonicity to obtain neuroprotective hypernatremia. However, as shown in our case, complete sodium equilibration between dialysate and patient, even when using high-volume CVVHDF, is unlikely because of residual kidney function and concomitant hypo- and isotonic IV medications. To obtain and maintain therapeutic hypernatremia in these conditions, the CRRT dialysate tonicity should be slightly higher than the targeted serum sodium.