Abstract

Laryngoscopy and tracheal intubation causes intense autonomic reflex responses such as tachycardia, hypertension and a rise in intraocular pressure (IOP). Rise in IOP is further compounded by the use of succinylcholine. Various drugs used to attenuate the rise in IOP are pre- treatment with non-depolarizing muscle relaxant, lignocaine, narcotics, nifedipine and nitroglycerine, but none is found to abolish it completely. To obtain haemodynamic response lignicaine, opiods, nitroprusside, nitroglycerine, vearpamil, nifedipine, esmolol, clonidine etc. have been used. AIMS AND OBJECTIVES: We investigated whether dexmedetomidine an α2 agonist could attenuate the rise in IOP after succinylcholine and intubation. Simultaneously, its effect on attenuation of haemodynamic response (Heart rate and MAP) to laryngoscopy and intubation was also evaluated. MATERIALS AND METHODS: Eighty patients without pre-existing eye disease undergoing general anesthesia was randomly premedicated by iv dexmedetomidine 0.6µg or saline. Heart rate (HR), mean arterial pressure (MAP), IOP (using Schioetz tonometer) was measured before, after the premedication, after thiopental, after succinylcholine, immediately after intubation and then every minute for 3 minutes. Statistical Analysis: descriptive and inferential statics using chi-square test, z- test and Wilcoxon sign rank test was done. Software used in the analysis was SPSS 17.0 version and Graph Pad Prism 5.0. Data was reported as mean value ± SD & p-value < 0.05 was considered as level of significance. RESULTS: Succinylcholine and intubation increased IOP in both the groups. However, in the dexmedetomidine group, it was not significantly different from baseline values (z value=0. 93, p=0. 358) and was significantly lower than in the control group (z =6. 644, p=0. 000). After intubation the MAP in the control group (z=17. 4, p=0. 000) was higher than that in the dexmedetomidine group (z=8, p=0. 000) and exceeded the baseline value (p<0.05). The heart rate also showed a less fluctuation in the dexmedetomidine group than in the control group. (z=7. 73, p<0.05 after succinylcholine and z=9. 22, p<0.05 after intubation) CONCLUSION: IV dexmedetomidine 0.6µg premedication is advantageous as it is found to be effective in reducing the rise in IOP. It is also beneficial in attenuating the haemodynamic response of succinylcholine, laryngoscopy and intubation to prevent its consequences.

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