Abstract
Introduction: The trigeminocardiac reflex has been reported in craniofacial, neurosurgery, ophthalmological surgeries, and recently at endovascular procedures. Therefore, it has been called by other names also as trigeminal depressor reflex, reflex vagal trigeminal, or oculocardiac reflex. It is provoked by the stimulation of branches of the trigeminal nerve and presents cardiovascular alterations such as hypotension, bradycardia, cardiac arrhythmias, which can lead to asystole. This reflex originates at the brainstem and occurs as a rare autonomic dysfunction triggered by the stimulation of baroreceptors. Some factors predispose the appearance of this type of reflex, such as hypercapnia, hypoxemia, superficial anesthetic depth, and acidosis, among others. During these procedures is recommended continuous monitoring of the ECG and PAM. It is always essential to know the patient and modify the risk factors, or even stop the stimulus notifying the surgeon, if there is no adequate response, anticholinergic therapy, such as atropine, and the use of vasopressors should be applied. Methods: We report a clinical case of an 18‐year‐old male with a history of 3 years of recurrent epistaxis diagnosed with a Juvenilenasopharyngeal angiofibroma stage IVB, who underwent diagnostic cerebral angiography for surgical planning. Results: Angiography was performed under conscious sedation. When we placed the JB2 diagnostic catheter in the external carotid artery, the patient presented bradycardia of 40bpm. The catheter was removed, and the heart rate improved; we made a second attempt again with bradycardia, for which atropine was administered, and continued with the procedure without incident. We evaluated the vascular supply to the tumor and ruled out the involvement of the ipsilateral internal carotid artery. An occlusion test was also performed, which was positive. No aneurysms were found during angiography. At the end of the angiography, the patient presented anisocoria and left hemiparesis, so due to the suspicion of a thromboembolic event, a new femoral approach was performed to assess the intracranial circulation we found adequate patency. A non‐contrast head CT was performed, a subarachnoid hemorrhage in the prepontine and the interpeduncular cistern was observed. Medications used for sedation were discontinued to assess his neurological status at that time with GCS of 12. 48 hrs later, the patient was neurologically intact and without sequelae. In the literature review, we did not find reports of intracranial hemorrhage as complications in nasopharyngeal angiofibroma with intracranial extension or secondary to the presentation of the trigeminocardiac reflex. However, we suspected that it could result from a transient elevation of arterial hypertension due to the administration of anticholinergic therapy. Conclusions: Neuroanesthesiologists and endovascular surgeons must be aware of its manifestations and management to avoid complications due to the presentation of this reflex.