Supraventricular tachycardia in a child undergoing strabismus surgery.

To the Editors: Supraventricular tachycardia (SVT) encompasses all types of tachycardia that start from above the bifurcation of the bundle of His with a heart rate ranging from 150 to 250 beats/min in children.1,2 Paroxysmal SVT occurs suddenly and can end rapidly.1 We describe a healthy 3-year-old boy who developed primary SVT during intraoperative extraocular muscle manipulation. Our patient underwent surgery to correct inferior oblique overaction. Under laryngeal mask airway anesthesia (propofol, fentanyl, ketorolac, isoflurane, and sevoflurane), the inferior oblique muscle was isolated using muscle hooks through a fornix incision. A 6-0 polyglactin suture was then placed through the muscle near its insertion. The patient then went into SVT. Contact with the muscle was stopped, but SVT continued at 227 beats/min. Carotid massage, ice placed on the forehead, and adenosine 1.5 mg 3 2 doses had no effect. A 12-lead electrocardiogram demonstrated features of reentry SVT (Figure). An additional 3 mg of adenosine restored sinus rhythm at 142 beats/min. One more incidence of SVT occurred, which was treated with 3 mg of adenosine. The inferior oblique muscle was re-isolated, and there was an episode of bradycardia treated with glycopyrrolate. The cardiac rhythm stabilized and surgery continued without complication. Subsequent transthoracic echocardiography was normal and the patient started propranolol 10 mg orally three times daily. In retrospect, a family history was positive for Wolff–Parkinson–White (WPW) syndrome in a first cousin. SVT is the most common form of arrhythmia in children and 90% is mediated through a reentry mechanism. This is facilitated by the presence of an accessory pathway in addition to the normal atrioventricular node and Purkinje system.3 Jacobson et al. detailed paroxysmal SVT during strabismus surgery in a 17-year-old with WPW syndrome.4 Paroxysmal reentrant SVT occurs in WPW syndrome using an accessory retrograde pathway that is manifest on electrocardiogram with a short PR interval and Delta waves.5 When these features are absent in reentrant SVT, presence of a concealed pathway is presumed.3 Our patient’s electrocardiogram did not have the characteristics of WPW and thus the reentrant SVT was mediated by a concealed pathway. It is speculated that in our case and in the patient with WPW, hypotension induced by anesthesia may have increased sympathetic tone, favoring conditions for a reentry circuit via the preexisting accessory pathway. The SVT may have been initiated by an ectopic escape beat in the setting of bradycardia from vagal stimulation induced by manipulation of the muscle. Acute treatment of SVT includes vagal maneuvers such as Valsalva maneuver and cold water immersion of the face. If these treatments fail, intravenous adenosine should be used; it works by inducing transient AV block that terminates SVT by interrupting the reentry pathway and allowing restoration of sinus rhythm.1 Final treatment options include elective cardioverison or procainamide. Chronic SVT treatment can involve the use of propranolol or other antiarrhythmic agents and catheter ablation.1