• Theresa Human, Rajat Dhar, Michael Diringer, and Adaeze Onuoha.
• Department of Clinical Pharmacy, Neurology/Neurosurgery Intensive Care Unit, Barnes-Jewish Hospital, Saint Louis, MO, USA.
• J Crit Care. 2012 Dec 1;27(6):745.e1-5.

PurposeThe aim of the study was to analyze the response to the vasopressin-receptor antagonist conivaptan in a large cohort of brain-injured patients with acute hyponatremia.Materials And MethodsThe natremic response (rise in serum sodium) to an initial bolus of conivaptan was retrospectively evaluated in 124 patients over a 3-year period in our neurosciences intensive care unit. Variables associated with this response were identified using linear regression.ResultsMedian pretreatment sodium was 132 mEq/L, and duration of hyponatremia before dose was 1 day. Median natremic response was +4 mEq/L (interquartile range, 2-7 mEq/L), measured a median of 9 hours (interquartile range, 6-12 hours) after conivaptan administration. This was associated with significant urine output (median, 2.6 L over 12 hours), with degree of aquaresis associated with natremic response (regression coefficient, B = 1.8 change in sodium per liter; 95% confidence interval, 1.3-2.4; P < .001). Seventy-four patients (60%) responded with a rise of at least 4 mEq/L. Response was predicted by higher baseline urine output (B = 0.018 per mL; 0.004-0.032; P = .01) and lack of oral fluid intake (B = 2.06; 0.44-3.68; P = .01) but not tonicity of intravenous fluids or creatinine clearance.ConclusionsConivaptan given as a bolus can effectively treat acute hyponatremia in brain-injured patients.Copyright © 2012 Elsevier Inc. All rights reserved.

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