Severe bradycardia in a child with an implanted vagus nerve stimulator undergoing laparoscopy -A case report-

Abstract

Background

Vagus nerve stimulation is an established therapeutic option for children with drug-resistant epilepsy who do not respond to other treatments. During surgical procedures, this therapy has various anesthetic implications and may result in critical respiratory and cardiac complications.

Case

We report the case of a 13-year-old child with an implanted vagus nerve stimulator who underwent laparoscopy-assisted gastrostomy tube placement under general anesthesia with the device activated. A severe episode of bradycardia occurred during pneumoperitoneum, which was successfully managed pharmacologically, without external device deactivation. The rationale for this management decision is discussed and reflections based on the clinical course are provided.

Conclusions

Perioperative management of vagus nerve stimulators must be individualized. Maintaining device activation may be reasonable in children with recent seizure activity, whereas temporary deactivation may be considered during procedures associated with a high risk of vagal reflex. However, in cases requiring immediate deactivation, pharmacological intervention may be necessary given the deactivation magnet latency.

The incidence of epilepsy in children is around 0.1%, with higher rates occurring in the first year, and up to one-third of children develop drug-resistant epilepsy. Risk factors associated with drug resistance include early onset, febrile seizures, status epilepticus, structural abnormalities, and certain epileptic syndromes (e.g., Lennox-Gastaut, West, or Dravet). Current therapeutic options include combination drug therapy, metabolic therapy (e.g., ketogenic diet), surgery, and neurostimulation strategies (e.g., vagus nerve stimulation therapy) [1,2].

Vagus nerve stimulation therapy is recommended for children aged ≥ 4 years with drug-resistant epilepsy who do not respond to other therapeutic measures. It consists of an implantable device that generates ascending electrical impulses that may modulate neuronal activity in different brain areas. Response rates (defined as ≥ 50% reduction in number of seizures) increase over time, reaching up to 60% at 2 years [1,3–5]. Complications are predominantly associated with device implantation, initial stimulation, and subsequent material replacement (very rare in non-device-related procedures). Most (66%) are respiratory (e.g., coughing or obstructive sleep apnea), whereas cardiac events (e.g., bradycardia or asystole) are extremely rare (≤ 0.1%) [3,4,6–11]. The vagal stimulator includes an external magnet that allows for temporary (extra) activation of stimulation during seizures. Sustained magnet application can suppress ongoing stimulation in case of device-related complications (e.g., laryngospasm or bradycardia), with baseline settings restored after magnet removal [4,5].

Perioperative management of children with implanted vagus nerve stimulators is increasingly common in daily clinical practice and may pose significant challenges owing to its anesthetic implications and potential associated perioperative complications. Special caution must be exercised regarding cardiovascular instability during procedures with high risk of vagal stimulation.

Written informed consent for the present publication was obtained from the child’s parents.

Case Report

We report the case of a 13-year-old boy with an American Society of Anesthesiologists physical status III and weighing 28 kg who was scheduled for laparoscopic-assisted gastrostomy tube placement under general anesthesia. His neonatal history included premature birth (32 weeks), low birth weight (1140 g), and congenital cytomegalovirus infection. His current medical history was notable for severe neurodevelopmental delay and drug-resistant epilepsy (Lennox–Gastaut syndrome), with approximately three seizures per day, managed with rufinamide and vagus nerve stimulation therapy (output current 2.25 mA in both normal and auto-stimulation modes, duty cycle 16%, and battery level 50%–75%). Additional comorbidities included profound hearing loss with bilateral cochlear implants, normal-pressure hydrocephalus, and subclinical hypothyroidism.

Upon arrival at the anteroom, an anesthetic safety checklist was completed, and the morning dose of antiepileptic medication was verified. Despite this, the patient had a tonic-clonic seizure in the preceding 3 h, which was resolved using the external magnet.

An opioid-free anesthetic technique was implemented upon arrival in the operating room. Anesthesia was induced using 5% sevoflurane, which was subsequently titrated to 1.5% for maintenance. Early boluses of ketamine (50 mg) and rocuronium (30 mg) were administered to facilitate tracheal intubation and controlled mechanical ventilation. A multimodal, opioid-sparing analgesic regimen was initiated using slow intravenous administration of dexmedetomidine (25 µg), magnesium sulfate (1 g), dexamethasone (8 mg), paracetamol (400 mg), dexketoprofen (30 mg), and ondansetron (3 mg). Intravenous fluid therapy consisted of Isofundin^® at 100 mL/h. Intraoperative monitoring showed stable parameters during induction and early maintenance, including an oxygen saturation of 99%, end-tidal CO₂ of 35 mmHg, heart rate of 75–90 bpm, systolic blood pressure > 90 mmHg, mean arterial pressure > 50 mmHg, perfusion index > 2%, bispectral index (BIS) values between 40 and 60, and core temperature between 36.5°C and 37.0°C.

During pneumoperitoneum insufflation at the onset of the surgical procedure, which involved a pressure of 10 mmHg and gas flow rate of 1.2 L/min, sinus bradycardia (40–50 bpm) was observed, prompting immediate pneumoperitoneum evacuation. Despite this measure, the heart rate decreased (30–40 bpm) and atropine 0.3 mg was administered. Sinus bradycardia then progressed to a nodal escape rhythm (20–30 bpm) and epinephrine 250 µg was promptly injected (before the atropine could take effect), resulting in a rapid increase in heart rate (160 bpm). Throughout the 60-s event, no electrocardiography ischemic changes, BIS abnormalities, or perfusion index disturbances were observed. Over the following 5 min, the heart rate gradually decreased (90–100 bpm). The procedure was resumed and completed uneventfully (total duration: 80 min). Finally, the child was extubated and transferred to the pediatric intensive care unit, where he remained awake and clinically stable for the entire 3-h stay.

Discussion

The anesthetic management of children with implanted vagus nerve stimulators requires careful consideration of multiple clinical aspects, including seizure control, device management, and procedure-specific risks. Several complications related to vagus nerve stimulators have been reported, such as upper airway collapse or obstruction; central apnea episodes; and arrhythmias (e.g., sinus bradycardia, atrioventricular block, asystole), which are rare but should be managed with pharmacological treatment and/or device deactivation when they occur [7,12–15]. In this case, several decisions shaped the perioperative management strategy.

The decision to maintain vagus nerve stimulator activation throughout the procedure was based on two considerations: first, the child experienced a tonic-clonic seizure within 3 h preoperatively, and second, institutional limitations in vagus nerve stimulator programming created uncertainty regarding postoperative device management. Although device deactivation is sometimes recommended for procedures with high vagal stimulation risk, such as laparoscopic surgery, the risk of perioperative seizures outweighed the potential cardiac risks in this specific case.

The opioid-free anesthetic technique, which included sevoflurane-based general anesthesia with multimodal analgesia, was employed to minimize respiratory depression and reduce seizure risk. Although sevoflurane has been associated with a lowered seizure threshold in some patients [12–14], we considered its use acceptable given that the vagus nerve stimulator was activated and the BIS monitoring was used to monitor anesthetic depth and potentially identify unexpected changes in cerebral electrical activity.

To our knowledge, this is the first reported case of severe bradycardia in a patient with vagus nerve stimulation therapy undergoing laparoscopic surgery. During pneumoperitoneum establishment, the insufflation pressure and flow rate were deliberately minimized to reduce the risk of vagal reflex, particularly given the recent seizure and probable increase in parasympathetic tone compounded by vagal stimulator activity. Despite these precautions, the patient developed bradycardia. Although the pneumoperitoneum was immediately evacuated and vagal reflex-induced bradycardia usually resolves with the cessation of the stimulus that triggered it, the heart rate continued to decline, progressing from sinus bradycardia to nodal escape rhythm.

The rapid progression of bradycardia (< 30 s from onset to nodal escape rhythm) necessitated immediate pharmacological intervention and rendered magnet-based device deactivation impractical. The magnet requires a sustained contact time for complete device inhibition, which would have been insufficient given the patient’s acute deterioration. Additionally, the vagus nerve stimulator operates in intermittent cycles, delivering electrical stimulation for brief periods, followed by rest intervals. The stimulation cycle may have coincided with the pneumoperitoneum-induced vagal reflex, creating a synergistic effect that exacerbated the bradycardia. Based on the clinical course, we hypothesized that the pneumoperitoneum-induced vagal reflex triggered the initial bradycardia, but subsequent progression to the nodal escape rhythm was likely exacerbated by concurrent vagus nerve stimulation.

In conclusion, perioperative management with vagus nerve stimulators must be individualized. In general, maintaining device activation may be reasonable in children with recent seizure activity, although clinicians must anticipate potential cardiac complications during high-risk procedures. The time required for magnet-mediated device inhibition may limit its usefulness in acute cardiac events, necessitating immediate pharmacological intervention when rapid clinical deterioration occurs. Regardless of the device management strategy, preparedness for both cardiac- and seizure-related complications is essential for safe perioperative care.