Real World Use of Hypertonic Saline in Refractory Acute Decompensated Heart Failure: A U.S. Center's Experience

Abstract

Objective To investigate real-world safety and potential therapeutic effect of hypertonic saline solution (HSS) for the management of refractory acute decompensated heart failure (ADHF). Methods Electronic medical records at a large urban academic hospital were queried for patients who were admitted with ADHF and received HSS. HSS was administered as 150cc of 3% hypertonic saline given concordantly with high dose loop diuretics. Statistical analysis was performed to identify significant changes in collected variables over time as well as predictors of improved fluid loss and renal function. Results A total of 58 HSS administration episodes were identified across 40 patients. On average, patients receiving HSS had high disease severity with sodium 131 mmol/L (IQR 125-134), creatinine 1.82 mg/dL (IQR 1.48 - 2.83), and BUN 63.5 mg/dL (IQR 40 - 83) prior to HSS administration. Median IV furosemide equivalents were 400mg/24 hours (IQR 190 - 800), 41% were receiving supplemental oxygen, and 64% were receiving inotropes/vasopressors. At the time of data collection 23 patients (57.5%) were deceased or discharged to hospice. All doses were 150mL of 3% HSS given as an intravenous infusion over 30 minutes, and patients received a median of 3 doses (IQR 2 - 7) during a treatment episode. Prior to HSS administration, serum sodium, chloride, and creatinine concentrations were deteriorating, but improved after HSS administration (p Figure , panel A & B). Serum sodium increased by 2 mmol/L (IQR 0.5 -3.5) at 24 hours after HSS. Both net fluid output and weight significantly improved post-HSS ( Figure , panel C & D). Inverse association was found between pre-HSS serum chloride (OR 0.37 per 10-unit change; 95% CI: 0.14 to 0.96; p = 0.041) and BUN (OR 0.74 per 10-unit change; 95% CI: 0.57 to 0.96; p = 0.024) and a positive treatment response (defined as increase in pre- to post-HSS net fluid output >2L in 24 hours). Serum sodium concentration was not predictive of treatment response, and no tested factors predicted the improvement of creatinine after HSS. There was no significant change in respiratory status observed in the pre-HSS versus post-HSS periods. Conclusion In a cohort of severely ill refractory ADHF patients, there were no adverse electrolyte or respiratory safety signals associated with HSS administration. Furthermore, HSS was associated with increased fluid and weight loss, as well as improvement in kidney function. These findings suggest additional rigorous study of HSS in the setting of ADHF is warranted.