Study protocol

Patients were randomized into two groups – lignocaine group (n = 25) and saline group (n = 25) using computer generated number table. The random number was enclosed in sealed opaque envelopes. After shifting the patient into operating room, the sealed envelope was opened by an anesthetic not involved in the study to prepare the drug for infusion according to randomization. Patients assigned to lignocaine group received an intravenous bolus of preservative free lignocaine (1% preparation) of 1.5 mg/kg just before induction of anesthesia with a subsequent continuous infusion of 1.5 mg/kg/h. Patients assigned to the control group received equal volume of saline. The hemodynamic parameters (heart rate [HR] and mean arterial pressure [MAP]), BIS, and MAC values were recorded at predetermined time intervals during preinduction (T1), postinduction (T2), postintubation (for first 5 min) (T3), during infiltration of nasal mucosa with solution of lignocaine and adrenaline (T4), during insertion of Hardy’s self-retaining nasal speculum (T5), at the time of sphenoid bone (T6), and seller ridge dissection (T7), during switching off the anesthetic agents (T8), at the time of extubation and every 5 min after extubation for 30 min.

The aim was to maintain hemodynamic parameters (MAP and HR) within 20% of baseline values. Any deviation from this was classified as hypertension (MAP >20% above baseline) or hypotension (MAP <20% below baseline) and tachycardia (HR >20% above baseline) or bradycardia (HR <40 bpm). Hypertension and/or tachycardia were treated with 1 μg/kg of intravenous fentanyl, if BIS was within the study range. Patients not responding to fentanyl were given esmolol 0.5–1 mg/kg as required. Hypotensive episodes were managed primarily with crystalloids, and 3 mg of i.v. mephentermine, if required. Atropine (0.5 mg) was used for bradycardia associated with hypotension.

All the anesthetic agents including desflurane, nitrous oxide, and drug infusion were stopped after the completion of surgery and packing of the nose. Residual neuromuscular blockade was reversed using neostigmine and glycopyrrolate after return of spontaneous respiratory effort. Tracheal extubation was performed after the patient responded to verbal commands, demonstrated purposeful movement and had adequate spontaneous respiration.

Time to emergence was defined as the period from switching off of anesthetic agents till tracheal extubation. Maximum MAP and HR attained during this period was recorded as emergence MAP and HR, respectively. ΔMAP (emergence MAP – baseline MAP) and ΔHR (emergence HR – baseline HR) were calculated as the difference between the emergence and baseline parameters. Percentage (%) increase in MAP and HR was also determined.

Patients with percentage increase in MAP ≥20% or those with emergence MAP >120 mmHg were treated with i.v. esmolol 0.5 mg/kg.

Cough during emergence was classified as (none-no cough; mild-single cough; moderate -more than one bout but unsustained that is <5 s cough; severe-sustained, and >5 s bouts of cough).[3] Emergence agitation was divided into four grades (1-calm and cooperative, calm easily arousable and follows command 2-restless, anxious but movements not aggressive, 3-agitated – frequent non purposeful movements; 4-very agitated – aggressive, pulls on tube and catheters; and requires physical restraint).[17]

The four emergence parameters (MAP, HR, cough, and agitation) were abbreviated into an aggregated score for QOE [Table 1].

Comparison of demographic data and patient characteristics between the two studied groups. Data expressed as mean (SD) or absolute numbers.