l Sciences & Humanities
Yagar, S., Yavas, S. and Karahalil, B. (2011) The Role of the ADRA2A C1291G Genetic Polymorphismin Response to Dexmedetomidine on Patients Undergoing Coronaryartery Surgery. Molecular Biology Reports, 38, 3383-3389.
ABSTRACT: Background: In our case we discussed the sedation made with dexmedeto-midine unresponsiveness and exaggerated response to propofol of patients with essential tremor. Case: 75 years old, male, without any co-existing disease, with essential tremor patient, planned deep brain stimulation operation under sedoanalgesia, one week before the operation the patient evaluated and was planned to perform brain magnetic resonance imaging (MRI) under sedation in the MRI unit. We performed sedation with fractional doses of 20 mg propofol than maintained the propofol infusion 0.5-1 mg/kg/hour. At the 20th minute the propofol infusion was stopped on the dropped of the patient’s blood pressure at 50/35 mmHg. After 20 mg efedrin was given intravenously, blood pressure was achieved to the basal levels in one minute. One week after we performed MRI and we gave only half dose of first time. Sleeping pattern analysis for obstructive sleep apnea or sleeping disorders was done for this patient. On the DBS day we decided to perform the procedure with dexmedetomidine. Initial bispectral index values 98%-99% (BIS aspect). After 20 minute neither BIS values, nor Ramsey changes. We maintained high doses dexmedetomidine but it didn’t worked, so we turned to propofol on 30th minute and after we performed 10 mg propofol, BIS values was 85%-88% throughout the operation. We gave 40-50 mg propofol totally throughout the procedure and RSS was 3-4. Discussion: Unresponsiveness of dexmedetomidine that we faced in our case may be by neurodegeneration of locus coeruleus and we could explain this exaggerated response to propofol of this patient on GABA receptor increased intensity.