(575) Occurrence of Hyperchloremia and Acute Kidney Injury After Hypertonic Saline in Neurologic Injury

Introduction: Hypertonic saline (HTS) can be used to treat elevated ICP after neurologic injury. Studies have associated hyperchloremia, acute kidney injury (AKI), and metabolic acidosis with HTS; however, the causal relationship has not been well defined. Our study objective was to classify the occurrence of hyperchloremia and subsequent outcomes in patients who received HTS boluses for elevated ICP.

Methods: A single center, retrospective chart review was conducted from November 1, 2020 to June 30, 2023 and included patients ≥ 18 years old admitted to a Neurosciences Intensive Care Unit who received HTS (3% or 23.4%) boluses for ICP control. Data collection included demographics, type of neurologic injury, number of HTS boluses, and sodium, chloride, and creatinine levels. The occurrence of AKI was the primary outcome. The secondary outcomes were the occurrence of metabolic acidosis and median changes in serum levels.

Results: This study evaluated 32 patients with a median age of 53 (33-64) years and 59.4% were male. The most common neurologic injury was an intracerebral hemorrhage (n = 15, 46.9%). During the HTS treatment period, 30 (93.8%) patients developed hyperchloremia, defined as chloride > 110 mEq/L, and 21 (65.6%) patients developed hypernatremia, defined as sodium > 145 mEq/L. The HTS treatment period was defined as 24 hours before the first dose until 72 hours after the last dose.

Three (9.4%) patients developed an AKI during the treatment period, with one occurrence preceding hyperchloremia. There was no statistically significant association between AKI and severe hyperchloremia, defined as chloride > 120 mEq/L, compared to non-severe hyperchloremia, defined as a chloride level of 110-120 mEq/L (p = 0.5681). Metabolic acidosis occurred in four (12.5%) patients, with two occurrences preceding hyperchloremia. The median maximum chloride level was 119 mEq/L (113-125) with a median change from baseline of 9 mEq/L (5-14). The median maximum sodium level was 149 mEq/L (143-155) with a median change from baseline of 7 mEq/L (4-12).

Conclusions: Our data show a low occurrence of AKI in patients who received HTS for the treatment of elevated ICP after neurologic injury despite a high occurrence of hyperchloremia; however, the small sample size encourages a larger study be conducted in this population.