A Comparative Study Between Intranasal and Intravenous Dexmedetomidine and Hemodynamic Responses During Endotracheal Intubation.

INTRODUCTION

Tracheal intubation and laryngoscopy may cause sympathetic stimulation, which can cause tachycardia and hypertension. To abolish the pressor response to laryngoscopy and endotracheal intubation, many medication combinations have been tried with varying degrees of efficacy.

MATERIALS AND METHODS

This randomized comparative study was double-blinded and included 106 subjects. Patients including those aged 18-60 belong to the American Society of Anesthesiologists (ASA) 1 and 2. These subjects were divided into two study groups. Group A received dexmedetomidine 0.5mcg/kg (200mcg diluted in 50ml syringe with normal saline (NS) up to 50cc 4mcg/ml) through an infusion pump over 40min before induction. Group B received dexmedetomidine intranasally (1mcg/kg) in undiluted which is prepared from parental preparation (100mcg/ml) and an equivalent dose of NS to the other group. The intranasal drug was dripped into both nostrils in equal volume using a 1ml syringe in a supine head-down position about 40min before induction. Both groups received an intravenous placebo and an intranasal placebo with normal saline.

RESULTS

In our study, intranasal and intravenous groups were compared. There was no statistically significant difference in hemodynamic variables like heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) between the two groups (majority p value >0.05). Hence both routes can be preferred for attenuation of pressor responses.

CONCLUSION

Study findings demonstrate dexmedetomidine can be utilized as a premedication to lessen hemodynamic surges during endotracheal intubation with more or less the same efficacy via intranasal and intravenous routes. This result could be attributable to the fact that both intravenous and intranasal dexmedetomidine stop central catecholamine levels from rising.