Trigeminovagal Reflex During Repair of a Nasal Fracture Under General Anesthesia

Abstract

The trigeminovagal reflex (TVR), probably best known as the oculocardiac reflex when it occurs during ophthalmic surgery, is manifested by cardiac bradyarrythmias. The TVR has been associated with intraoperative deaths [1] and can occur with non ophthalmic surgery, primarily maxillofacial surgery [2]. We report the occurrence of TVR after repair of a nasal fracture under general anesthesia. Case Report A healthy, 36-yr-old woman was scheduled for closed reduction of a traumatic nasal fracture. Before the induction of general anesthesia, her heart rate (HR) was 84 bpm, blood pressure was 140/60 mm Hg, and arterial oxygen saturation (SaO2) was 98%. General anesthesia was induced with the IV administration of fentanyl (150 [micro sign]g), lidocaine (100 mg), and propofol (150 mg), and 80 mg of IV succinylcholine was used to facilitate endotracheal intubation. Anesthesia was maintained with 1.0%-1.5% sevoflurane, 70% nitrous oxide, and 30% oxygen. No hemodynamic changes were apparent during the 10-min surgical procedure, the SaO2 was 100%, and the end-tidal carbon dioxide level was 32-36 mm Hg, as measured by capnography. After surgery, a malleable plastic splint was formed across the nasal bridge to stabilize the fracture site. Manual pressure was applied over the nose to shape the splint. Seconds after application of the splint, the patient's HR decreased from 72 to 32 bpm. The surgeons were notified, and the immediate administration of atropine 200 [micro sign]g IV increased the HR to 120 bpm. Within 2 min, the HR returned to 90 bpm. Further manipulation of the nasal splint resulted in a bradycardia of 25 bpm. Release of the pressure increased the HR to 60-70 bpm without the administration of atropine. Manual pressure was applied only over the nose, and at no time was there pressure over the eye. One further episode of bradycardia (HR 45 bpm) was noted before completion of the procedure. No bradycardic episodes occurred in the postanesthesia care unit, and the patient was discharged after 45 min. Discussion The literature describing bradycardia mediated via the TVR during ophthalmic surgery is extensive. The neurologic pathway defining the reflex is well described: the afferent limb of the reflex arc involves neuronal transmission from the orbital structures to the ciliary ganglion, the ophthalmic division of the trigeminal nerve, and the sensory nucleus of trigeminal nerve near the fourth ventricle. The efferent limb travels via the vagus nerve to the myocardium [3]. However, the maxillary (II) and mandibular (III) divisions of the trigeminal nerve may also contribute to the afferent pathway of the reflex arc, and TVR-mediated bradyarrythmias have been described during mandibular and maxillary osteotomies [4]. Even simple maneuvers, such as mouth opening, may cause life-threatening TVR-mediated asystole in the anesthetized patient [5]. The nasal bridge is innervated by sensory branches of the maxillary (II) division of the trigeminal nerve. In our patient, external pressure applied over the nasal bridge after surgery while forming the nasal splint triggered the TVR arc. We could not immediately explain the first episode of bradycardia. However, when the second episode occurred, a cause-and-effect relationship between the external pressure applied over the nasal bridge and the decrease in HR was appreciated. Hypoxia and hypercarbia increase the incidence of TVR, as does light anesthesia [6]. Our patient was not hypoxic or hypercarbic. The end-tidal concentration of sevoflurane was <0.5% because we anticipated the emergence from anesthesia. The low anesthetic concentration may have contributed to the TVR in our patient. Other factors associated with an increased incidence of TVR include the use of drugs such as halothane, vecuronium, atracurium, succinylcholine, fentanyl, alfentanil, and sufentanil [7]. Our patient received a relatively small (2.5 [micro sign]g/kg) dose of fentanyl on induction of anesthesia without causing a decrease in HR. Similarly, no bradycardia was noted after the injection of succinylcholine. Classically, the TVR is reported to "fatigue" with repeated application of the triggering stimulus [8]. It is possible that the moderate bradycardia noted with the last episode and the normal HR seen in our patient after application of the splint, despite some persistent pressure over the nose, was a result of such fatigue. In summary, we describe the occurrence of the TVR during the application of a malleable splint for the repair of a nasal fracture. Communication with the surgical team is essential, and cessation of the precipitating stimulus is the first and most important therapeutic step. Afferents other than the ophthalmic (I) division of the trigeminal nerve can be responsible for the reflex arc, and the TVR should be part of the differential diagnosis in all cases of unexplained bradycardia during operations on the face.