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Middle East Journal of Anesthesiology 2011-Jun

Clevidipine for controlled hypotension during spinal surgery in adolescents.

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Joseph D Tobias

Sleutelwoorden

Abstract

BACKGROUND

Clevidipine is an ultra-shorting acting, intravenous calcium channel antagonist of the dihydropyridine class. Metabolism by blood and tissue esterases results in a half-life of 1-2 minutes thereby allowing easy titration by i.v. administration. We present preliminary experience with this novel agent to provide controlled hypotension (CH) in a cohort of adolescents undergoing posterior spinal fusion.

METHODS

The records of patients < or = 18 years of age who received clevidipine for CH were retrospectively reviewed. Demographic data included age, weight, gender, and co-morbid 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) as well as the MAP and HR during the clevidipine infusion. Adverse effects related to clevidipine included excessive hypotension (need to discontinue the infusion or the need for a fluid bolus or administration of a vasopresor), tachycardia (20% increase in HR or the administration of a beta-adrenergic antagonist) and elevated serum triglyceride level.

RESULTS

The study cohort included 20 patients, ranging in age from 14 to 18 years and in weight from 46 to 96 kgs. To provide acceptable conditions for evoked potential monitoring, a total i.v. anesthetic technique was used. Propofol was started at 100 microg/kg/min and titrated to maintain the bispectral index at 40-60. Remifentanil was started at 0.1 microg/kg/min and increased up to 0.3 microg/kg/min as needed to control MAP. If the MAP was > or = 65 mmHg, clevidipine was added to maintain the MAP at 50-65. The clevidipine infusion was started at 0.5-1 microg/kg/min and increased in increments of 0.5-1 microg/kg/min every 2-3 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 1-5 microg/kg/min (2.9 +/- 0.7 microg/kg/min). With the administration of clevidipine, HR increased from a baseline of 76 +/- 14 to 92 +/- 11 beats/minute (p < 0.05). The HR increase was > or = 20 beats/minute in 4 patients. Intermittent doses of metoprolol were used in 3 patients to control the HR increase. No excessive hypotension was noted. A triglyceride level was drawn in 6 patients who received clevidipine with propofol and was elevated in 3 patients (> or = 150 mg/dL, high level 328 mg/dL). 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 effectively controlled MAP and provided CH. Mild tachycardia was noted in some patients with the occasional need for a beta-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. Should inadvertent hypotension occur, its short duration of action offers an additional advantage over several other i.v. antihypertensive agents.

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