Navigating Challenges: A case report of Brugada Syndrome and Difficult Airway Management
Author's: Freitas, Rita1,2; Gordillo, Inmaculada1,3
Affiliations: 1 – Anesthesiology Department - Unidade Local de Saúde Lisboa Ocidental (ULSLO);
2 - Anesthesiology Resident;
3 - Anesthesiologist Assistent.
Corresponding Author:
Rita Freitas
Lisbon, Portugal
Contact information: ritafreitas1993@gmail.com or +351 918387839
ABSTRACT
Background: Brugada Syndrome is an autossomal dominant genetic disorder characterized by abnormal findings on the electrocardiogram, an increased risk of ventricular tachyarrhythmias and sudden cardiac death. The prevalence in the population is 0,1 to 1% and it is 2 to 9 times more likely in men. Many drugs have been reported to induce arrhythmias in these patients, and so should be avoided by the anesthesiologist. But what if in addition to Brugada Syndrome, which precludes the use of local anesthetics, the patient also has a known difficult airway?
Case Report: A 63-year-old man, with dyslipidemia and an implantable cardioverter-defibrillator placed for Brugada Syndrome, was proposed for bilateral ear canaloplasty. He also had a history of difficult orotracheal intubation in past surgery, but easy face mask ventilation. As a strategy, we chose to perform a rapid sequence induction after preoxygenation, with fentanyl, etomidate and rocuronium, given the impossibility of approaching the airway with the patient awake. He was intubated with videolaryngoscope at first attempt. Anesthesia was maintained with sevoflurane; a second peripheral access was placed, and the radial artery was catheterized. During surgery, to maintain hemodynamic stability, atropine and isoprenaline boluses were administered, followed by isoprenaline infusion. The magneto was available in case of need. The surgery was uneventful, and the patient was successfully extubated.
Discussion: Brugada Syndrome should be familiar to the anesthesiologist in order to manage it correctly: a meticulous pre-anesthetic evaluation, planning and perioperative management should be carried, with prompt diagnosis and treatment of arrhythmias. In this case, an additional challenge of the difficult airway existed, with the impossibility of performing local anesthesia of the oropharynx. Decisions must be individualized, based on current guidelines, and the planning of the anesthetic approach must encompass several hypotheses.
Keyword's: BRUGADA SYNDROME; DIFFICULT AIRWAY; ARRHYTHMIA; LOCAL ANESTHETICS; GENERAL ANESTHESIA;
INTRODUCTION
Since 1992, when the Brugada brothers first described that the association of right ventricular conduction delay and right precordial ST-elevation would predispose to ventricular arrhythmias, Brugada Syndrome has become recognized as an important cause of syncopal episodes and sudden cardiac death. This syndrome is responsible for up to 40% of these cases in a structurally normal heart [1].
Brugada Syndrome is a cardiac abnormality of transmembrane conduction with autosomal dominant inheritance, variable expression and incomplete penetrance (which explains why 60% of patients with this syndrome have no affected family member). Although it has been linked with mutations in about ten genes, the most common mutation is in the SCN5A gene, coding for the cardiac sodium channels insensitive to tetrodotoxin, rendering enhanced inactivation of these channels [2]. There are three different electrocardiographic patterns in Brugada Syndrome: type 1 is characterized by pronounced elevation of the J point, a coved-type ST segment, and an inverted T wave in V1 and V2; type 2 has saddleback ST-segment elevation by more than 1 mm and type 3 shows ST segment elevation less than 1mm. The type 1 pattern is diagnostic of Brugada Syndrome. Malignant arrhythmia events may be triggered by different metabolic factors (fever, pain, electrolyte imbalances) and pharmacological drugs (antiarrhythmic drugs such as flecainide, procainamide and propafenone; psychotropic drugs such as amitriptyline, clomipramine and lithium; and local anesthetics such as procaine, bupivacaine). The imposition of the parasympathetic autonomic nervous system and vagal tone has also been implicated in the development of ST segment alterations [3]. There are several drugs commonly used by the anesthesiologist that can have proarrhythmic effects and interactions in this syndrome. Local anesthetics and propofol are considered strong triggers for the onset of arrhythmic events, and for this reason, Brugada syndrome is a major challenge during anesthesia management [4].
An additional challenge arises when the same patient presents with a difficult airway. Since all difficult airway guidelines and algorithms establish that, in the presence of an established difficult airway, it is recommended to approach the patient with spontaneous ventilation and vigil, this is compromized when the topicalization of the oropharynx and laryngeal structures with local anesthesia cannot be performed.
This case report targets the challenges faced by the anesthesia providers in securing a safe airway in a patient with a known difficult airway and Brugada Syndrome for a procedure where regional anesthesia was not an option, with the additional difficulty that local anesthesia could not be performed.
CASE PRESENTATION
We present the case of a 63-year-old man, ASA III, with obliterative ear exostosis, proposed for elective bilateral canaloplasty surgery. As medical history, this patient had dyslipidemia and an implantable cardioverter-defibrillator (ICD) placed for Brugada Syndrome. In the context of previous cardiorespiratory arrest, the study was carried out to diagnose Brugada Syndrome type II, placing an ICD as secondary prophylaxis of malignant arrhythmia events.
Beyond this, he also had a history of difficult orotracheal intubation with direct laryngoscopy in a previous procedure, but easy facemask ventilation was documented. In the previous procedure, orotracheal intubation was possible with the support of nasofibroscopy.
Regarding the pre-anesthetic evaluation, a chest X-ray and ECG were made, and an analytical study was conducted with blood count, biochemistry and coagulation without alterations. He also went to a cardiology consultation before the surgery, where the correct functioning of the implantable electronic cardiac device was verified.
In the operating room, before the arrival of the patient, all material, drug preparation and safety checklist checks were carried out. Acknowledging an anticipated difficult airway, the mainstay approach should be an awake tracheal intubation, with maintenance of spontaneous ventilation. However, given the impossibility of performing oropharynx local anesthesia, an alternative strategy was chosen.
We used ASA standard monitoring and placed an arterial line before anesthesia induction. We also applied the self-adhesive pre-applied electrode pads before any drug administration.
We then decided to perform a rapid sequence induction after adequate preoxygenation with fentanyl, etomidate and rocuronium. Easy ventilation with a face mask was confirmed, ensuring adequate oxygenation of the patient. The intubation was managed using the videolaryngoscope, securing the airway at the first attempt. Anesthesia was maintained with sevoflurane and remifentanil infusion, and a second peripheral access was placed. During surgery, atropine and isoprenaline boluses were administered, followed by isoprenaline infusion, to maintain hemodynamic stability. In figure 1 it is possible to see some alterations found in the electrocardiographic tracing, namely in the T wave. The magneto was available in case of need. The surgeon was also asked to use bipolar electrocautery with minimal energy as possible and for as short a period of time as possible. The surgery was uneventful, and the patient was successfully extubated, after reversal of the neuromuscular block with sugammadex, fully awake. Total surgery and anesthesia times were 270 minutes and 320 minutes, respectively, and no complications were registered.
In the postanesthesia care unit, vigilance and monitoring were maintained, with special attention to periods of extreme bradycardia or other dysrhythmias, as well as the treatment of the main complications, such as pain, nausea and vomiting. After meeting the discharge criteria, he was transferred to the ward, where he was discharged the following day.
Fig. 1 – Intraoperative recording of electrocardiographic findings.
DISCUSSION
During anesthesia practice, drugs that interact with cardiac ion channels are routinely used. The evidence regarding the anesthetic management of Brugada Syndrome patients is still limited at present. Regarding general anesthesia, safe drugs include midazolam, opioids and etomidate. For maintenance, volatile anesthetics, opioids and muscle relaxants can be safely administered [3,5].
Patients with Brugada Syndrome are at risk of ventricular fibrillation and sudden cardiac death during the perioperative period. There are several triggers that can initiate these events, like medications, surgery, fever, electrolyte disturbances and changes in autonomic system tone. So, to avoid perioperative arrhythmias, it is mandatory to optimize dyselectrolytemia, and maintain adequate depth of anesthesia and normothermia [6].
Brugada Syndrome should be familiar to the anesthesiologist in order to manage it correctly: a meticulous pre-anesthetic evaluation, with risk stratification, planning and perioperative management should be carried out, with prompt diagnosis and treatment of arrhythmias. In this specific case, the presence of an anticipated difficult airway presented as an additional challenge regarding the impossibility of performing topical anesthesia of the upper airway and subsequent awake patient fibreoptic intubation. Predicting that adequate facemask ventilation would be achieved, we opted for a rapid sequence induction to provide excellent intubation conditions at first attempt. Videolaryngoscopyenabled successful orotracheal intubation and a subsequent secure airway approach. As an alternative, the fiberscope was available in the operating room to be used after induction.
Regarding the drugs chosen for the anesthetic induction, we opted for the ones considered safe for administration in Brugada Syndrome patients. No events were recorded using sevoflurane in this population [7].
CONCLUSION
An individualized decision-making process should be based on current guidelines, and the planning of the anesthetic management must encompass several hypotheses. Timely detection of cardiac arrhythmias and immediate treatment are very important. By avoiding agents or conditions that may exacerbate arrhythmias in Brugada Syndrome patients during anesthesia, we were able to manage our case uneventfully.
REFERENCES
[1] D. Levy, C. Bigham, et al. Anaesthesia for patients with hereditary arrhythmias part I: Brugada syndrome. BJA Education, 18(6): 159e165 (2018).
[2] M. Ribeiro, A. Cunha, et al. Anesthesia Management of a Patient with Brugada Syndrome for an Urgent Procedure. Revista da Sociedade Portuguesa de Anestesiologia. VOL. 28 - No 1 - 2019.
[3] M. Ranucci. Challenge of Anesthesia Management in Brugada Syndrome. Anesthesiology, V 132 • NO 3 March 2020
[4] Cuttone G, Martucci G, Napoli R, Tigano S, Arcadipane A, Pappalardo F, et al. Anesthesiological management of Brugada syndrome patients: A systematic review. Saudi J Anaesth 2023;17:394-400.
[5] Guler N, Kati I, Demirel CB, Bilge M, Eryonucu B, Topal C. The effects of volatile anesthetics on the Q–Tc interval. J Cardiothorac Vasc Anesth. 2001; 15: 188–91. doi:10.1053/jcan.2001.21949.
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[7] Guler N, Kati I, Demirel CB, Bilge M, Eryonucu B, Topal C. The effects of volatile anesthetics on the Q–Tc interval. J Cardiothorac Vasc Anesth. 2001; 15: 188–91. doi:10.1053/jcan.2001.21949.
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