Abstract: FR-PO665
Hypernatremia Induced by Treatment for Hypokalemia in a Patient with Sjögren Syndrome and Renal Tubular Acidosis
Session Information
- Fluid and Electrolytes: Clinical - Potassium, Sodium, Water
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid and Electrolytes
- 902 Fluid and Electrolytes: Clinical
Author
- Shimizu, Hideaki, Daido Hospital, Nagoya, Japan
Introduction
Hypokalemia and metabolic acidosis are severe complications of renal tubular acidosis (RTA) in Sjögren's syndrome. The concentration of sodium in the plasma water should equal the concentration of sodium plus potassium in the total body water. The sodium concentration is not always considered when treating hypokalemia.
Case Description
A 60-year-old women presented with general weakness, hypotension, hypokalemia, metabolic acidosis, and acute kidney injury. Her blood pressure was 60/44mmHg, and her heart rate was 89/min.
Na+ 144 K+ 1.5 mEq/L, Cl- 114 mEq/L, glucose 166 mg/dL, BUN 65.9 mg/dL, Cr 2.34 mg/dl, pH 7.052, PCO2 36.2, PO2 321, and HCO3- 9.6 mEq/L. Urinary electrolytes Na+ 41 mEq/L, K+ 12.2 mEq/L, Cl- 32 mEq/L, pH 6.5, Osmolality 244 mOsm/kg.
The patient was intubated because of respiratory muscle weakness from severe hypokalemia. She was treated with intravenous potassium chloride (KCl 400 mEq) and isotonic fluid for the treatment of hypovolemic shock. This solution was actually hypertonic because of its high potassium concentration: Na+ 110 mEq/L, and K+ 147 mEq/L, in a total of 2.6 liters.
After 18 hours the patient developed hypernatremia (Na+ 161 mEq/L), but her serum potassium had normal sized (K+ 4.6 mEq/L). Her urinary measurements were as follows: Na + 40 mEq/L, K+ 52.7 mEq/L, Cl- 82 mEq/L, and osmolality 405 mOsm/kg.
After the hypertonic fluid was changed to a hypotonic type, she recovered.
She was also found to have Sjögren’s syndrome after a positive screen for anti-Lo, and anti-Ra antibodies. A positive Schirmer’s test and a renal biopsy also suggested Sjögren’s syndrome. She was discharged without complications.
There is no physical examination or other vital signs.
Discussion
This case indicates that serum sodium concentration should be carefully monitored in patients with hypokalemia and acute kidney injury induced by distal RTA receiving intravenous potassium chloride therapy and hypertonic fluid, which contain high levels of potassium. We should keep this complication in mind when treating severe hypokalemia.
Clinical Course