ABSTRACT
The trigeminovagal reflex manifests as a sudden onset of bradycardia, hypotension, and cardiac arrest in response to the stimulation of the trigeminal nerve. The incidence of trigeminovagal reflex in maxillofacial surgical procedures is approximately 1.6%. We report a case of asystole in a pediatric patient in whom a dental mouth gag triggered the trigeminovagal reflex during oral surgery. The patient was a 5-year-old boy who was scheduled to undergo extraction of maxillary supernumerary teeth. After tracheal intubation, anesthesia was maintained with sevoflurane and remifentanil. At the beginning of the surgery, his mouth was opened with a dental mouth gag, and electrocardigram showed asystole for 20 seconds. Thereafter, his heart rate spontaneously returned to basal value within 60 seconds. Since sufficient mouth opening was required to conduct the surgery, his mouth was opened again with the gag. When the interincisal distance exceeded about 40 mm, his heart rate suddenly decreased, but spontaneously returned to baseline within 60 second. The subsequent anesthetic course was uneventful.
Subject(s)
Heart Arrest , Oral Surgical Procedures , Anesthesia, General/adverse effects , Child , Child, Preschool , Heart Arrest/etiology , Humans , Intraoperative Complications , Male , Mouth , Oral Surgical Procedures/adverse effectsABSTRACT
Monoamine oxidase (MAO) deficiency is an X-linked hereditary disease characterized by spontaneous deletion of MAO-A and/or MAO-B on the X chromosome. Here, we describe the first reported case of a patient with MAO-A and MAO-B deficiency managed under general anesthesia in dental treatment. The patient was aged 11 years old when he was scheduled for dental treatment. He was diagnosed with MAO-A and MAO-B deficiency on genetic testing at 2 years of age. He was not given premedication, and standard monitoring with noninvasive blood pressure monitoring, pulse oximetry, and ECG was instituted. We also preemptively prepared a cardioverter-defibrillator. General anesthesia was induced with propofol 46 mg (2 mg/kg), then rocuronium 10 mg (0.4 mg/kg) and remifentanil 0.30 µg/kg/min were administered via separate infusion pumps. Orotracheal intubation was performed without complications. Anesthesia was maintained uneventfully with a continuous infusion of remifentanil 0.15-0.2 µg/kg/min and propofol 5.0-7.0 mg/kg. Fresh gas flow included oxygen and air. End-tidal CO2 concentration was maintained at around 35 mmHg throughout the procedure. We administered sugammadex 92 mg (4 mg/kg) for reversal of neuromuscular blockade and the patient was extubated. We achieved successful anesthetic management without any appreciable clinical signs of fatal arrhythmias in this patient with MAO-A and MAO-B deficiency.