Vasopressin-induced hyponatremia during mean arterial pressure augmentation in acute spinal cord injury: A multicenter retrospective cohort study.

Abstract

Background: MAP augmentation is a guideline-recommended intervention in acute spinal cord injury (SCI), and vasopressin can be used to achieve mean arterial pressure (MAP) goals. Vasopressin could contribute to hyponatremia in SCI, but this relationship is poorly described.

Methods: This was a multicenter, retrospective, observational cohort of patients with acute SCI who received vasopressin only for MAP augmentation and developed hyponatremia. Patients were excluded if vasopressin was used for <6 h or for an alternative indication (e.g. shock states). The primary outcome was the probability hyponatremia was caused by vasopressin, determined using the Naranjo Adverse Drug Reaction Probability Scale.

Results: Twenty patients with SCI received vasopressin for MAP augmentation and 17 (85%) developed hyponatremia. Seventy percent of patients received an American Spinal Injury Association Impairment Scale (AIS) classification at admission: AIS A (42%), AIS B (50%), and AIS C (8%). MAP augmentation (mean goal of 87 (±7) mm Hg) was maintained for 5 (±2) days. The median Naranjo score was 7 (range 4-9), constituting a "probable" association of vasopressin with hyponatremia. Hyponatremia (Na <135 mEq/L) developed within 30 (±20) hours of vasopressin initiation, with a nadir at 129 (±4) mEq/L. Sodium declined by 8 mEq/L on average for every 24 h of vasopressin exposure. Hyponatremia resolved 12 (±9) hours after vasopressin discontinuation. Five patients were rechallenged with vasopressin and 4 (80%) re-developed hyponatremia.

Conclusion: Vasopressin used for MAP augmentation was associated with hyponatremia in patients with SCI who received it strictly for MAP augmentation and resolved after discontinuation. Providers should exercise caution when selecting vasopressin for MAP augmentation in acute SCI.