JOURNAL ARTICLE

Clevidipine for controlled hypotension during spinal surgery in adolescents

Joseph D Tobias, Daniel G Hoernschemeyer
Journal of Neurosurgical Anesthesiology 2011, 23 (4): 347-51
21623231

BACKGROUND: Clevidipine is an ultrashort-acting, intravenous calcium channel antagonist. Metabolism by blood and tissue esterases results in a half-life of 1 to 2 minutes. We present preliminary experience with this novel agent to provide controlled hypotension (CH) in a cohort of adolescents undergoing spinal surgery.

METHODS: The records of patients ≤18 years of age who received clevidipine for CH were retrospectively reviewed. Demographic data included age, weight, sex, and comorbid disease processes. Information regarding clevidipine included the initial infusion rate, time to achieve the target mean arterial pressure (MAP), the maintenance infusion rate, the average infusion rate, and the duration of administration. Hemodynamic information included the starting MAP and heart rate (HR) and the MAP and HR during the clevidipine infusion. Charts were reviewed for adverse effects related to clevidipine including excessive hypotension (MAP ≤50 mm Hg, the need to discontinue the infusion or the need for a fluid bolus or administration of a vasopressor) or the administration of a β-adrenergic antagonist.

RESULTS: The study cohort included 20 patients, ranging in age from 14 to 18 years and in weight from 46 to 96 kg. A total intravenous anesthetic technique (propofol, remifentanil, and dexmedetomidine) was used. When the MAP was ≥65 mm Hg, clevidipine was added to maintain the MAP at 50 to 65 mm Hg. The clevidipine infusion was started at 0.5 to 1 μg/kg/min, and increased in increments of 0.5 to 1 μg/kg/min every 2 to 3 minutes to achieve the desired MAP. The target MAP was achieved within 5 minutes in 15 of the 20 patients and within 10 minutes in the other 5 patients. The maintenance infusion rate of clevidipine varied from 1 to 5 μg/kg/min (2.9±0.7 μg/kg/min). With the administration of clevidipine, HR increased from a baseline of 76±14 to 92±11 beats/min (P<0.05). The HR increase was ≥20 beats/min in 4 patients. Intermittent doses of metoprolol were administered to 3 patients. No excessive hypotension was noted. When the clevidipine infusion was discontinued, MAP returned to baseline within 5 minutes in 16 of the 20 patients and within 10 minutes in the other 4 patients.

CONCLUSIONS: Clevidipine maintained the MAP at 50 to 65 mm Hg and provided CH. Mild tachycardia was noted in some patients with the occasional need for a β-adrenergic antagonist. No episodes of excessive hypotension were noted. Given its short half-life, clevidipine can be rapidly titrated to provide CH when changing levels of sympathetic stimulation may occur.

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