In our case, light mechanical stimuli to the dura mater induced severe bradycardia. Since topical application of lidocaine to the dura surface prevented bradycardia, it was speculated that it was the response via TCR. This reflex pathway activates parasympathetic vagal neurons of the sinus node or atrioventricular node of the heart, resulting in bradycardia [4]. When TCR was defined as a decrease of HR lower than 60 beats/min accompanied by hypotension with a decrease in mean blood pressure of 20% or more, the incidences of TCR and cardiac arrest due to TCR were 11% and 2.4%, respectively, in cases of surgery in the cerebellopontine angle [3]. It has also been reported that cardiac arrest due to TCR occurs in 2.3% of cases of unruptured cerebral aneurysm clipping surgery [5]. Therefore, TCR-induced bradycardia is a symptom that should be dealt with as soon as possible. Predisposing factors for TCR include hypoxemia, hypercapnia, preoperative use of beta-blockers or calcium channel blockers, light anesthesia, children, and narcotic use [6]. Additionally, remifentanil has been reported to decrease the threshold for vagal excitation [7]. In our case, preoperative use of beta-blockers, intraoperative use of calcium channel blockers (verapamil), and intraoperative use of remifentanil were considered as predisposing factors.
When encountering severe bradycardia due to TCR, the first step of treatment is interruption of the manipulation. If the bradycardia or hypotension persists, atropine should be administered. If atropine is not effective, adrenaline administration may be considered [8]. In addition, nerve blocks and topical anesthesia of the dura mater may be effective. In ophthalmic surgery, peribulbar or retrobulbar block has been reported to reduce the incidence and severity of TCR [8]. In brain surgery, Chigurupati et al. reported a case showing the effectiveness of a trigeminal nerve block by a local anesthetic at the site where it branches from the brainstem for preventing TCR-induced bradycardia [9]. However, the use of local anesthetics near the brainstem can lead to irreversible complications [10]. It has also been reported that topical anesthesia of the dura mater with lidocaine-soaked gelfoam or lidocaine infiltration was effective for preventing TCR [11]. The dura mater was anesthetized by infiltrating 1–2 ml of 1% lidocaine with adrenaline between the leaves of the dura adjacent to the middle meningeal artery with a 25-gauge needle and tuberculin syringe in addition to covering with small gelfoam soaked in lidocaine 1%.
In our case, topical anesthesia of the dura surface with lidocaine prevented bradycardia induced by light mechanical stimuli to the dura mater. In previous reports, tetracaine, cocaine, and bupivacaine were used as local anesthetics [11]. We thought that lidocaine was more suitable because of its rapid effect. These methods may be a good way to suppress TCR without affecting the brainstem.
The limitation of this case report is that it was not determined which is more useful for preventing TCR-induced bradycardia since topical anesthesia of the dura surface and atropine administration were performed simultaneously. In addition, since there have been many reports showing that atropine and local anesthesia are effective in preventing bradycardia due to TCR [2, 4, 8, 10, 11], the novelty of our case may be limited. Regarding local anesthesia, local anesthetics were used for nerve block in most reports, and there has been only one report on topical anesthesia of the dural surface for preventing TCR-induced bradycardia. Therefore, we think that our case has educational value to make many anesthesiologists aware of the usefulness of topical anesthesia of the dural surface for preventing TCR-induced bradycardia.