Abstract: SA-OR47
Plasma Sodium Correction Rates in Patients with Severe Hyponatremia Treated with Hypertonic Saline with and without Desmopressin
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical Advances
October 26, 2024 | Location: Room 4, Convention Center
Abstract Time: 04:40 PM - 04:50 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- AlShanableh, Zain, UPMC, Pittsburgh, Pennsylvania, United States
- Ralchenko, Anna, UPMC, Pittsburgh, Pennsylvania, United States
- Yabes, Jonathan Guerrero, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States
- Sterns, Richard H., University of Rochester School of Medicine and Dentistry, Rochester, New York, United States
- Weisbord, Steven D., University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States
- Rondon Berrios, Helbert, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States
Background
Co-administration of desmopressin and hypertonic saline 3% (HTS) from the outset of treatment (the “DDAVP clamp”) has been suggested to prevent inadvertent overcorrection of hyponatremia, but the effectiveness and safety of this strategy remain uncertain.
Methods
We identified adult patients hospitalized between 7/1/18 and 6/30/23 at four UPMC hospitals with a plasma sodium (PNa) ≤120 mEq/L at admission or during hospitalization who were treated with HTS, excluding patients on renal replacement, eGFR <15 ml/min/1.73m2, plasma glucose >300 mg/dl, prior desmopressin treatment, or absence of PNa data within 12 h of starting HTS. Between-group comparisons were performed using t-test and Chi-square or Fisher exact test.
Results
A total of 184 patient admissions (57.6% female, mean age 60.6 years) met inclusion and exclusion criteria. Hyponatremia was chronic in 92.9%; leading causes were SIAD (51.6%), hypovolemia (25.5%), and low solute intake (15.8%); and 20.1% had seizures. Cases treated with HTS and desmopressin (n=46) were compared to cases treated with HTS without desmopressin (n=138). Despite a lower baseline PNa (110.5±6.4 vs. 115.1±7.2 mmol/L, p<0.001), correction by >8 mEq/L (6.5% vs. 27.5%, p=0.006) or >10 mEq/L (0% vs. 15.2%, p=0.011) within the first 24 hours was significantly less frequent in the desmopressin group than in the non-desmopressin group. Furthermore, presumably to prevent or reverse overcorrection, desmopressin was given to 40% of patients in the non-desmopressin group within 48 h of HTS initiation. Hospital mortality (6.5% vs. 6.5%, p>0.99), length of hospital (12.2 d vs. 11.8 d, p=0.810) and ICU stays (5.8 d vs. 5.5 d, p=0.678), fluid overload (8.7% vs.9.6%, p>0.99), and worsening of hyponatremia (2.2% vs. 1.5%, p>0.99) were similar in the two groups (HTS and desmopressin vs. HTS alone) but PNa was checked significantly more often in the desmopressin group (20.7 vs. 17.4, p<0.001). No cases of osmotic demyelination syndrome were identified.
Conclusion
Treating severe hyponatremia with HTS and desmopressin was associated with lower rates of rapid correction without significant adverse events compared to HTS alone.