Observational studyThe journal of spinal cord medicine2026
Vasopressin-induced hyponatremia during mean arterial pressure augmentation in acute spinal cord injury: A multicenter retrospective cohort study.
Observational study in The journal of spinal cord medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Factors associated with hyponatremia in patients with acute spinal cord injury: a systematic review and meta-analysis.Frontiers in medicine · 2026Pooled it
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundMAP 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.
methodsThis 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 (
resultsTwenty 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.
conclusionVasopressin 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.
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