Asystole due to stimulation of the supraorbital nerve: abrupt and potentially fatal presentation of the trigeminocardiac reflex

Abstract

We present a case of sudden asystole that was elicited via the trigeminocardiac reflex in a patient undergoing surgery for a frontal sinus fracture. Asystole occurred after mild stimulation of the supraorbital nerve during dissection along the superior orbital rim. Anticholinergics were administered and lidocaine-soaked gauze was applied to the exposed wound. The patient was an athlete and had pre-existing sinus bradycardia. We hypothesise that the severe reflex response was associated with his underlying increased vagal tone. When performing surgery in patients with increased vagal tone, preventative measures to diminish the trigeminocardiac reflex are recommended. Further studies are needed.

Background

The trigeminocardiac reflex (TCR) can manifest as cardiovascular abnormalities that include bradycardia, hypotension, arrhythmia and, in severe cases, asystole.^1–3 This reflex has been mainly described in strabismus surgery, where it is known as the oculocardiac reflex as well as neurosurgical procedures.² It has not been reported after manipulation of the periosteum of the superior orbital rim. In the case described herein, supraorbital nerve stimulation during open reduction of a fracture of the anterior wall of the frontal sinus resulted in asystole due to the TCR.

Case presentation

A 13-year-old adolescent boy (height, 168 cm; weight, 59 kg) was scheduled to undergo open surgical reduction and fixation of a fracture of the anterior wall of the frontal sinus after being struck in the eyebrow by a baseball (figure 1). The patient had been training as a baseball player for 5 years. A preoperative ECG showed sinus bradycardia (50 beats/min). He denied any corresponding symptoms such as fatigue, dizziness or syncope. There was no evidence of increased intracranial pressure. He was not receiving parasympatheticomimetic medication and had no underlying cardiac disease or prior incidence of adverse cardiovascular events during exercise. Preoperative chest radiography and routine laboratory testing were normal. His blood pressure and heart rate on the day before surgery were 130/72 mm Hg and 54 beats/min, respectively.

Figure 1.

Facial bone CT (A) with three-dimensional surface rendering (B) demonstrates a fracture of the anterior wall of the left frontal sinus.

The patient received no premedication. Intraoperative monitoring included ECG, sphygmomanometry, pulse oximetry, bispectral index (BIS) and capnography. The patient’s vital signs before induction of anaesthesia were as follows: blood pressure, 123/71 mm Hg; heart rate, 62 beats/min and oxygen saturation, 99%. General anaesthesia was induced with 120 mg of intravenous propofol, continuous remifentanil infusion and 50 mg of intravenous rocuronium. Immediately after endotracheal intubation, the patient’s blood pressure was 135/70 mm Hg and heart rate was 70 beats/min. Surgery was initiated by extending the wound medially with an incision. The periosteum was then incised and a subperiosteal dissection was performed to expose the fracture. While carefully dissecting around the superior orbital rim, asystole suddenly occurred on the ECG when mild traction was applied to the periosteum near the supraorbital nerve. The blood pressure and heart rate just before the asystole occurred were 94/55 mm Hg and 68 beats/min, respectively. Surgery was immediately halted and the ECG returned to normal sinus rhythm with a heart rate of 70–75 beats/min. The duration of asystole was approximately 3–4 s. At this point, blood pressure was 91/55 mm Hg, end-tidal partial pressure of CO₂ was 33 mm Hg, BIS score was 49, expiratory concentration of sevoflurane was 3.0%–3.2% and target effect-site concentration of remifentanil was 3.0 ng/mL. Surgery was resumed after adequate depth of anaesthesia and haemodynamic stability was confirmed; however, when the relevant periosteum was slightly elevated again, sudden asystole recurred (figure 2). Surgery was then halted, and sinus rhythm with a heart rate of 70 beats/min was restored.

Figure 2.

The patient’s ECG shows a sudden asystole.

Treatment

A significant portion of the superior orbital rim at the fracture site was dissected, exposing a portion of the supraorbital nerve; therefore, a gauze soaked in 4% lidocaine solution was placed over the dissected wound for approximately 5 min. After administration of 0.6 mg of intravenous atropine, careful and gentle subperiosteal dissection was resumed. The patient’s heart rate remained between 73 beats/min and 88 beats/min and other haemodynamic parameters remained within normal range. There were no additional adverse events during the remainder of the operation or emergence from anaesthesia (figure 3).

Figure 3.

The beginning of wound closure.

Outcome and follow-up

The patient’s vital signs and ECG were unremarkable in the postanesthesia care unit. His postoperative ECG showed sinus rhythm with a heart rate of 60 beats/min. Later, during his stay in the general ward, his pulse rate was 58–65 beats/min.

Discussion

This report presents a severe case of the TCR which occurred intraoperatively following mild stimulus of the supraorbital nerve during fracture repair of the anterior wall of the frontal sinus under general anaesthesia. Asystole without preceding bradycardia was induced due to stretching of the supraorbital nerve during subperiosteal dissection along the superior orbital rim. We considered ECG skin electrode detachment as a possible cause but the plethysmography confirmed asystole. A recently introduced definition of the TCR suggested that only a >20% reduction in heart rate is required; blood pressure decline is an additional but non-essential criterion. The case reported here is consistent with this definition.^{3 4}

The TCR involves a stimulus to the afferent trigeminal pathway that is transmitted along the short internuncial nerve fibres in the reticular formation to the efferent pathway of the motor nucleus of the vagus nerve.^{1 3} As a result, cardioinhibitory parasympathetic vagal activation leads to clinical manifestations. The oculocardiac reflex is a peripheral type of TCR. It can be elicited by a stimulus transmitted through the ophthalmic branch of the trigeminal nerve, which commonly occurs when an extraocular muscle is stretched during strabismus surgery.¹ The supraorbital nerve is a division of the ophthalmic nerve and leaves the orbit through the supraorbital notch or foramen (figure 4).⁵ Avoiding stimulation of the supraorbital nerve is difficult when superior orbital rim dissection is required to reduce a fracture of the anterior wall of the frontal sinus fracture.⁵ In this regard, a sudden and severe TCR response may have been elicited despite cautious surgical technique in our case due to the individual physiology of the patient.

Figure 4.

After exiting the orbit on the superior orbital rim, the branches of supraorbital nerve lie deep to the orbicularis and frontalis muscles, in close approximation to the periosteum of the supraorbital ridge. Drawing courtesy of HK.

Sinus bradycardia in an athletic individual requires no further evaluation or intervention and is generally attributed to increased vagal tone caused by exercise conditioning.⁶ This patient had not undergone a previous evaluation of pulse rate, therefore, it is unknown whether the sinus bradycardia was pre-existing or trauma related. He had no arrhythmia or relevant symptoms. Paediatric patients with sinus bradycardia who are asymptomatic and healthy do not require any further treatment.⁷ Therefore, we hypothesise that pre-existing increased vagal tone contributed to the abrupt occurrence of asystole even with a mild stimulus of the supraorbital nerve.¹ Although no studies have yet investigated higher underlying vagal tone and elicitation of the TCR, increased vagal tone has been suggested as a predisposing factor.¹ The increased vagal tone may be attributed to parasympathetic agonists medication, increased intracranial pressure, myocardial infarction, carotid sinus pressure and valsalva manoeuvres in addition to endurance training in athletes.^{8 9}

One of the first and most important steps in TCR management is immediate cessation of the responsible stimulus.^{1 2} In addition, intraoperative factors such as light anaesthesia, hypercapnia and hypoxia should be corrected.¹ Administration of anticholinergics may be required when bradycardia is severe or persistent despite removal of the stimulus. When the TCR is refractory to conventional treatment, vasopressors such as epinephrine may be required.^{1 2} In the case reported here, lidocaine-soaked gauze was applied to the surgical wound based on expectation of local absorption and subsequent neural blockade of the exposed responsible nerve. In addition, as asystole occurred without preceding bradycardia, it was considered a safe and necessary treatment option. Although neural blockade with a local anaesthetic is not considered totally preventative,^{1 10} we suggest it is necessary, as evidenced by this case. It has been reported that temporary pacing was applied to the management for the chronic form of TCR.¹¹

In summary, this case exemplifies a severe manifestation of the TCR. Abrupt asystole resulted from intraoperative supraorbital nerve stimulation in a patient with pre-existing sinus bradycardia. Based on previous recommendations, adequate depth of anaesthesia was confirmed and anticholinergics were administered. In addition, lidocaine-soaked gauze was applied to the exposed nerve that triggered the efferent limb of the reflex. We hypothesise that pre-existing increased vagal tone may have contributed to this unusual occurrence of the TCR and suggest that active preventative methods may be needed in such patients. Further studies are needed.

Learning points.

• The trigeminocardiac reflex (TCR) can manifest as cardiovascular abnormalities which can be abrupt and fatal and require careful monitoring and prompt management.

• Pre-existing increased vagal tone may contribute to elicitation of the TCR by mild nerve stimulation; active prevention is suggested in such patients.

• Inhibition of the TCR by local anaesthetic neural blockade has not been established as a preventative method; however, its application according to the clinical situation may be considered.