Introduction: Acute spinal cord injury (SCI) is complicated by hemodynamic instability due to disruption of sympathetic pathways and unopposed vagal stimulation. Previous guidelines recommended maintaining a mean arterial pressure (MAP) > 85 mmHg for the first 7 days after injury to improve neurologic outcomes. However, more recent guidelines recommend a MAP between 75–80 mmHg and 90-95 mmHg for the first 3-7 days. While catecholamine vasopressors are recommended to achieve MAP goals, the safety of adjunctive vasopressin in SCI remains unstudied. SCI patients are predisposed to hyponatremia due to autonomic dysfunction and inappropriate anti-diuretic hormone secretion. Vasopressin’s anti-diuretic effects may exacerbate hyponatremia, potentially worsening outcomes. This study aims to evaluate the safety of adjunctive vasopressin use in acute SCI patients undergoing MAP augmentation. Methods: This was a retrospective study of ICU patients with SCI admitted between January 2021 to December 2024. Patients were included if they had a documented MAP goal > 85 mmHg, consistent with institutional practice based on available guidelines during the study period, and received catecholamine vasopressors with vasopressin for at least 1 hour. Patients with concomitant shock states, including hemorrhagic shock, or an American Spinal Injury Association (ASIA) grade E were excluded. Patient characteristics, vasopressor use, sodium trends, and MAP goal attainment were analyzed with descriptive statistics. Results: Of 97 patients with SCI who received vasopressin, 28 met inclusion criteria (mean age 48.3 ± 20.4 years; 76.9% male; 89.3% White). A decline in sodium was observed in 21 patients (75.0%), with a mean drop of 8.9 mEq/L among those affected. Three patients (10.7%) experienced severe hyponatremia (Na 80% of the time in 36.7% patients. The average time from catecholamine initiation to vasopressin was 26.8 ± 38.6 hours, with MAP augmentation lasting 5.6 ± 1.8 days. Conclusions: When vasopressin was used for MAP augmentation in patients with acute SCI, a decline in sodium was observed; however, severe hyponatremia was uncommon. These findings raise concerns about the risks of vasopressin and support further investigation into its role in MAP augmentation in patients with acute SCI.
Davidson et al. (Sun,) studied this question.