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Abstract: FR-PO583

Management of Critical Hypernatremia During Continuous Renal Replacement Therapy and Septic Shock

Session Information

Category: Trainee Case Report

  • 902 Fluid and Electrolytes: Clinical

Authors

  • Valenzuela, Harol S., Medical University of South Carolina, Charleston, South Carolina, United States
  • Fulop, Tibor, Medical University of South Carolina, Charleston, South Carolina, United States
  • Marshall, Anna, Medical University of South Carolina, Charleston, South Carolina, United States
Introduction

The concept of osmotic stability in the critically ill during continuous renal replacement therapy is insufficient explored. Herewith, we are reporting a case of extreme hypernatremia (serum sodium [SeNa+] 182 mEq/L) with septic shock and acute kidney injury addressed with continuous renal replacement therapy (CRRT) and simultaneous hypertonic saline (HTS) administration.

Case Description

A 52-year-old male suffered a motor bicycle accident with subarachnoid hemorrhage and traumatic right below-the-knee amputation[FT1] . On the 17th day of hospitalization he suffered acute decompensation with increased work of breathing and decreased alertness. He required emergency intubation with mechanical ventilation and 3 pressor agents to maintain acceptable BPs. Initial laboratory studies revealed acute kidney injury with serum creatinine (SeCr) 3.6 mg/dL (normal baseline), BUN 142 mg/dL and sodium 177 mEq/L. With intravenous fluids, SeCr improved to 3 mg/dL while SeNa+ rose to 182 mEq/L. Due to subsequent anuria, resistant hypoxia and escalating vasopressor requirements, a decision was made to start CRRT in continuous hemofiltration modality. To address co-morbid hyperosmolar state, HTS with 3% saline was added to ensure a predictable rate of SeNa+ correction; correction for serum protein content (5 mg/dL) was achieved by multiplying predicted SeNa+ by 0.95 to calculate in vivo SeNa+.

Recovery was complicated by hypotonic polyuria and central diabetes insipidus (DI), attributable to subarachnoid hemorrhage.

Discussion

While presence of DI was difficult to recognized with anuria and AKI but undoubtedly was responsible for hypernatremia on presentation. Premixed CRRT fluids are hypotonic (Na+ 140 mEq/L) by default, when considering the presence of serum protein content. Excessive drops of SeNa+ and BUN likely would have caused harm in our index case without concurrent HTS administration. Management of dysnatremic CRRT protocols represent an important and emerging field of critical care nephrology.

CVVHD and Electrolytes
Days on CVVHDBFR/Therapy fluid doseHypertonic (3%) saline infusionSeNa+SeOsmSeCrBUNUOsmUNa+
Day-1250 mL/min
4L/hrs
250 mL/hr182 mEq/L443
Mosm/kg
3 mg/dL139 mg/dLAnuricAnuric
Day-2250 mL/min
4L/hrs
200 mL/hr169 mEq/L372
Mosm/kg
2.9 mg/dL119 mg/dLAnuricAnuric
Day-3250 mL/min
4L/hrs
150 mL/hr160 mEq/L343
Mosm/kg
2.6 mg/dL93 mg/dLAnuricAnuric
Day-4250 mL/min
4L/hrs
100 mL/hr152 mEq/L312
Mosm/kg
0,8 mg/dL21 mg/dLOliguricOliguric
Day-5CRRT stop3% saline stop144 mEq/L318
Mosm/kg
0.6 mg/dL11 mg/dL122 mOsm/kg<20 mmol/L
Day-6DDAVP 1 mcg Q12 hrsD5W 100 mL/hr149 mEq/L320
Mosm/kg
0.6 mg/dL9 mg/dL544 mOsm/kg130 mmol/L