Intravenous lidocaine attenuates distention of the optical nerve sheath, a correlate of intracranial pressure, during endotracheal intubation.

Abstract

By preventing hypoxia and hypercapnia, advanced airway management can save lives among patients with traumatic brain injury. During endotracheal intubation (ETI), tracheal stimulation causes an increase in intracranial pressure (ICP), which may impair brain perfusion. It has been suggested that intravenous lidocaine might attenuate this ICP response. We hypothesized that adding lidocaine to the standard induction medication for general anesthesia might reduce the ICP response to ETI. Here, we measured the optical nerve sheath diameter (ONSD) as a correlate of ICP and evaluated the effect of intravenous lidocaine on ONSD during and after ETI in patients undergoing anesthesia. This double-blinded, randomized placebo-controlled trial included 60 patients with American Society of Anesthesiologists I or II physical status that were scheduled for elective surgery under general anesthesia. In addition to the standard anesthesia medication, 30 subjects received 1.5 mg/kg 1% lidocaine (0.15 mL/kg, ONSD<inf>lidocaine</inf>) and 30 received 0.15 mL/kg 0.9% NaCl (ONSD<inf>placebo</inf>). ONSDs were measured with ultrasound on the left eye, before (T<inf>0</inf>), during (T<inf>1</inf>), and 4 times after ETI (T<inf>2-5</inf> at 5-min intervals). Compared to placebo, lidocaine did not significantly affect the baseline ONSD after anesthesia induction measured at T<inf>0</inf>. During ETI, the ONSD<inf>lidocaine</inf> was significantly smaller (β=-0.24 mm P=0.022) than the ONSD<inf>placebo</inf>. At T<inf>4</inf> and T<inf>5</inf>, the ONSD<inf>placebo</inf> increased steadily, up to 20 min after ETI, but the ONSD<inf>lidocaine</inf> tended to return to baseline levels. We found that the ONSD was distended during and after ETI in anesthetized patients, and intravenous lidocaine attenuated this effect.