The present study was a randomised double-blind study which was conducted after the approval from the Institutional Ethics Committee (KIMS/KIIT/IEC/65/2018). One hundred patients consenting to participate were included. The study was registered with Clinical Trials Registry- India (CTRI): CTRI/2018/07/0148. This study was conducted in Kalinga Institute of Medical Sciences, Bhubaneswar, Odisha, India from November 2018 to August 2020.

By adopting the reported IOP measurements associated with different doses [10], i.e., 16.9, 17.04, 18.75 and within group variance of 3.28 at 1% level of significance and 80% of the minimum power of study, the required sample size is 24 in each group. Therefore, 100 subjects were randomised into four groups in the study. Patients aged 18-60 years with ASA Physical Status (PS) class I or II, with normal IOP posted for non-ophthalmic surgery under general anaesthesia were included in the study.

Patients with anticipated difficult airway, psychiatric disorders, acute or chronic eye diseases, with raised intracranial pressure, receiving any drug known to alter IOP, pregnant or lactating patients or hypertensive patients receiving any antihypertensive drugs were excluded. During the process, patients requiring prolonged laryngoscopy and more than one attempt to intubation were also excluded from the study.

Randomisation was done using computer software research randomiser and patients were allocated to four different groups [Table/Fig-1]:

[Table/Fig-1]:

CONSORT flow chart.

Group A (n=25) received dexmedetomidine 0.6 μg/kg

Group B (n=25) received dexmedetomidine 0.8 μg/kg

Group C (n=25) received dexmedetomidine 1 μg/kg

Group D (n=25) received NS

As per the randomisation list, either 0.6 μg/kg or 0.8 μg/kg or 1 μg/kg injection dexmedetomidine was diluted to 20 mL with NS or 20 mL of NS only (placebo) were prepared by a resident doctor who was not a part of the study. After shifting to OT, monitors were attached and the prepared solution was started using syringe pump. The solution was infused intravenous (IV) over 10 minutes. IV fluids was started with Ringer Lactate (RL) solution at the rate of 4 mL/kg/hr simultaneously. Monitoring included three lead ECG, pulse oximetry, capnography and non-invasive blood pressure. Patients were premedicated with Inj. nalbuphine 0.1 mg/kg IV. After pre-oxygenation for three minutes patients were induced with injection propofol 2 mg/kg and succinylcholine 1.5 mg/kg IV. After cessation of fasciculations, laryngoscopy followed by intubation was done. Maintenance of anaesthesia was done with isoflurane and injection vecuronium. IOP was measured using Schiotz tonometer by an ophthalmologist at different points in time. To avoid the diurnal variation associated with the changes in IOP, all the surgeries that were taken for the study were posted in the morning. Systemic side-effects like bradycardia and hypotension were treated with either atropine or ephedrine respectively. In case of unresponsive bradycardia and/or hypotension the solution was stopped and the patients were dropped from the study.

The IOP were measured as:

Data were collected, tabulated, coded in MS excel sheet and the statistical analysis was carried out using standard statistical software Statistical Package for the Social Sciences (SPSS) 22.0. All the qualitative parameters were represented as frequency and percentage whereas continuous parameter will be reported as mean±standard deviation. As regard to continuous variables; student’s t-test was used. One-way ANOVA was used to find out association between two categorical variables. The p-value was considered as significant if <0.05 and highly significant if <0.001.

There were no significant differences (p>0.05) among the groups regarding age, weight, duration of laryngoscopy and the preoperative IOP [Table/Fig-2].

The mean IOP decreased after dexmedetomidine premedication in groups A, B and C (p<0.0001). Propofol administration further decreased IOP in all the groups. There was statistically significant difference in IOP between the control and study groups (p<0.0001). Succinylcholine administration and intubation caused a spike in the mean IOP of all the groups. The increase in IOP in control group was statistically significant when compared to the other groups (p<0.0001). But a comparison between the study groups showed no statistical significance even though the reduction in IOP was more in group C. The rise in IOP produced due to succinylcholine, laryngoscopy and intubation persisted upto five minutes after intubation. The difference in mean IOP between control and study groups remained statistically significant even after five minutes after intubation [Table/Fig-3,4].

[Table/Fig-4]:

Distribution of Intraocular Pressure (IOP) in all groups (p<0.05 as compared to control group).

Hypertension was seen in seven patients in the control group and two patients in group C. The hypertension seen in group C was very short lived, not warranting any intervention. Hypotension was seen in four patients of group C, requiring Ephedrine and fluid boluses and two patients of group B, requiring a single bolus of Ephedrine. Bradycardia was seen in one patient in each of groups B and C, not warranting any treatment [Table/Fig-5].

In the present study, dexmedetomidine in all three doses were equally effective in preventing the rise of IOP associated with succinylcholine administration. However, the side-effects associated with the higher doses was a limiting factor.

The changes in IOP between the control and study groups correlated well with the studies done by Mowafi HA et al., and Pal CK et al., who also noted a similar trend in IOP after dexmedetomidine administration [8,10]. Jaakola ML et al., found a 34% reduction in IOP after a dexmedetomidine premedication alone [9]. On the contrary, Lee YY et al., found no effect of dexmedetomidine on IOP when supplemented with Isoflurane anaesthesia probably because their study used a much lower dose than the present study [11].

Dexmedetomidine when injected at the rate of 1 mcg/kg/hr is known to cause initial hypertension and a reflex bradycardia [7]. In the present study only two patients were recorded with such events may be because of premedication with inj. glycopyrolate and slow infusion of the drug over 10 minutes. Hypotension has been recorded in four patients in group C requiring Ephedrine and fluid boluses and in two patient of group B requiring a single bolus of Ephedrine each. The hypotension was probably exaggerated with induction dose of propofol therefore requiring treatment.

Dexmedetomidine in all three doses were equally effective, but a better haemodynamic stability was achieved with a dose of 0.6 μg/kg/IV with a significant reduction in IOP. Sedation produced by dexmedetomidine in group C might have unblinded the clinician administering the anesthetic agents but as an ophthalmologist was measuring the IOP, it did not affect the results.

Using a fixed dose of propofol caused undesired hypotension in group C which could have been avoided, but it was necessary for adequate blinding. Serum catecholamine could have been measured to get a better correlation but it could not be done because of the cost constraints.

Premedication with dexmedetomidine is effective in attenuation of the rise in IOP associated with succinylcholine administration. It also significantly obtunded the sympathetic response to laryngoscopy and intubation. But a more desirable haemodynamic stability though not statistically significant was achieved with the dose 0.6 μg/kg. Therefore dexmedetomidine 0.6 μg/kg IV premedication can be used for attenuating the rise in IOP associated with succinylcholine administration in situations where rise of IOP may be detrimental.