Prevention of trigeminocardiac reflex-induced severe bradycardia during cerebral aneurysm clipping surgery by topical anesthesia of the dura surface and atropine administration: a case report

Background Trigeminocardiac reflex (TCR) by stimulation of the sensory branch of the trigeminal nerve induces transient bradycardia and hypotension. We report a case in which light mechanical stimulation to the dura mater during brain surgery induced severe bradycardia. Case presentation A 77-year-old woman with bradycardia-tachycardia syndrome was scheduled for clipping of an unruptured left middle cerebral artery aneurysm. General anesthesia was performed with propofol, remifentanil, and rocuronium. Before starting surgery, the function of the pyramidal tract was examined by motor evoked potential. Transcranial electric stimulation for motor evoked potential induced atrial fibrillation and tachycardia. Continuous administration of landiolol was started and verapamil was used for tachycardia. During detachment of the dura mater from the bone, an electrocardiogram suddenly showed sinus arrest for 6 s. Immediately after the manipulation was interrupted, a junctional rhythm appeared. However, light touch to the dura mater induced severe bradycardia again, and atropine was therefore administered. In addition, the dura surface was anesthetized with topical lidocaine infiltration. After that, light touch-induced bradycardia was prevented. Conclusions We experienced a case of severe bradycardia during surgery due to TCR caused by light mechanical stimulation to the dura mater. Topical anesthesia of the dura surface and atropine administration were effective for preventing TCR-induced bradycardia.

Accelerated Idioventricular Rhythm Following Intraoral Local Anesthetic Injection During General Anesthesia

Some anesthetic agents or adjunct medications administered during general anesthesia can cause an accelerated idioventricular rhythm (AIVR), which is associated with higher vagal tone and lower sympathetic activity. We encountered AIVR induced by vagal response to injection-related pain following local anesthetic infiltration into the oral mucosa during general anesthesia. A 48-year-old woman underwent extraction of a residual tooth root from the left maxillary sinus under general anesthesia. Routine preoperative electrocardiogram (ECG) was otherwise normal. Eight milliliters of 1% lidocaine (80 mg) with 1:100,000 epinephrine (80 μg) was infiltrated around the left maxillary molars over 20 seconds using a 23-gauge needle and firm pressure. Widened QRS complexes consistent with AIVR were observed for ∼60 seconds, followed by an atrioventricular junctional rhythm and the return of normal sinus rhythm. A cardiology consultation and 12-lead ECG in the operating room produced no additional concerns, so the operation continued with no complications. AIVR was presumably caused by activation of the trigeminocardiac reflex triggered by intense pain following rapid local anesthetic infiltration with a large gauge needle and firm pressure. Administration of local anesthetic should be performed cautiously when using a large gauge needle and avoid excessive pressure.

Abstract 1122‐000193: Intracranial Bleeding in a Juvenile Nasopharyngeal Angiofibroma Stage IVb

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.

Penanganan Trigeminocardiac Reflex (TCR) selama Anestesi untuk Bedah Saraf

Trigeminocardiac reflex (TCR) is a unique brain stem reflex that manifests as negative cardio-respiratory perturbations. The trigeminocardiac reflex (TCR) is defined as the sudden onset of parasympathetic dysrhythmia, sympathetic hypotension, apnea, or gastric hypermotility during stimulation of any of the sensory branches of the trigeminal nerve. Clinically, the TCR has been reported in all the surgical procedures in which a structure innervated by the trigeminal nerve is involved. This reflex is largely reported in skull base surgeries/interventions; however, in recent times, it has been also linked with many neurosurgical, neurointerventional procedures, non-neurosurgical and non-surgical conditions. This reflex presents with many cardiovascular changes that can create catastrophic complications, worse outcome as well as diagnostic dilemmas. Although, there is an abundant literature with reports of incidences and risk factors of the TCR; the physiological significance and function of this brainstem reflex has not yet been fully elucidated. In addition, there are complexities within the TCR that requires examination and clarification. If a CTR occurs, it can risk factor identification and modification, depth of anesthesia assessment, prophylactic treatment with either vagolytic agents or peripheral nerve block in case of peripheral manipulations of the nerve, careful cardiovascular monitoring during anesthesia, especially in those with a risk factor for TCR, treatment of the condition when it occurs: cessation of the manipulation, and administration of vagolytic agents and adrenaline. Therefore, this narrative review intends to elaborate on its mechanisms, definition, pathophysiology, manifestations, diagnosis and management.

Efficacy of transcutaneous cardiac pacing for transient asystole caused by trigeminocardiac reflex: illustrative case

BACKGROUND Trigeminocardiac reflex (TCR) is a brainstem reflex caused by stimulation of the trigeminal nerve, which results in bradycardia, hypotension, and asystole. TCR can occur during any neurosurgical procedure. Initially, it is managed via the immediate removal of the stimulus from the trigeminal nerve. If asystole persists after intravenous atropine or glycopyrrolate, chest compression or transcutaneous cardiac pacing may be considered. The authors present the first case of TCR that was successfully managed with transcutaneous cardiac pacing. OBSERVATIONS A 51-year-old man presented with aneurysmal subarachnoid hemorrhage. Although he had no history of cardiac disease and there were no abnormal findings on electrocardiography, transient asystole due to TCR occurred during craniotomy. The patient’s heart rate spontaneously recovered after the immediate discontinuation of the procedure. The authors completed aneurysm clipping with transcutaneous cardiac pacing because intravenous atropine was not effective in preventing TCR. There were no complications associated with intraoperative asystole or transcutaneous cardiac pacing, and the patient was discharged without neurological deficits. LESSONS TCR can be appropriately managed with the immediate discontinuation of intraoperative procedures. Furthermore, transcutaneous cardiac pacing may be considered for persistent TCR with poor response to intravenous atropine or glycopyrrolate.

A rare appearance of the trigeminocardiac reflex during resection of posterior parasagittal meningioma

Background: Although a well-recognized phenomenon of the tentorium and posterior fossa, the trigeminocardiac reflex (TCR) has been rarely reported during surgery involving the posterior falx cerebri. Case Description: We present the case of a 63-year-old woman who underwent repeat resection of an atypical parasagittal meningioma involving the posterior falx. During resection, TCR was repeatedly elicited during manipulation and coagulation of the falx. Air embolism and cardiac etiologies were initially considered while TCR was not suspected, given the location. Ultimately, TCR was recognized when asystole self-resolved upon cessation of stimulus and due to its reproducibility. Conclusion: Awareness by the anesthesiologist and neurosurgeon of the possibility of TCR during falcine procedures can help with rapid identification to avoid a potentially catastrophic outcome.