Anaesthetic management in patients with high-risk Brugada syndrome
Editor—We read with interest the case report from Dr Edge and colleagues,1 and would like to report the successful management of two cases with Brugada syndrome and focus on risk evaluation of proarrhythmia, postural change and neostigmine administration. During anaesthesia of Brugada syndrome, many factors may precipitate a significant risk of malignant arrhythmias and cardiac arrest.Both patients were asymptomatic with no medical history of cardiac disease or family history of sudden death. Preoperative echocardiography was normal, and the ECG over the third intercostal space and the ECG following pilsicainide administration revealed obvious augmentation of ST segment elevation in leads V1–V4, without QT prolongation. Electrophysiological studies, without prior medication, induced ventricular fibrillation (VF) and systolic pressure <40 mm Hg, and defibrillation restored sinus rhythm. These findings led to a definite diagnosis as high-risk Brugada syndrome.
Before induction of general anaesthesia, the 12-lead ECG was continuously monitored, along with routine monitoring and cardioverter-defibrillator pads. An automated external defibrillator and an i.v. drip infusion of the ß-stimulator isoproterenol were prepared, in case ventricular dysrhythmias developed.2 No pre-anaesthetic medication was required. General anaesthesia was induced with thiamylal 4 mg kg–1, and tracheal intubation was facilitated by vecuronium 0.1 mg kg–1. Anaesthesia was maintained with isoflurane and nitrous oxide 66% in oxygen.
Case 1. A 51-yr-old man with a left-sided coral-shaped calculus underwent percutaneous nephrolithotripsy twice. During the operations, three types of postural change were required—from supine to lithotomy, lithotomy to prone and prone to supine position.
Case 2. A 56-yr-old man with a mandibular fracture underwent plate fixation and plate removal procedure after 1 yr. Nasotracheal intubation was required because of previous oral surgery.
At the end of the operation, atropine 0.02 mg kg–1 and neostigmine 0.02 mg kg–1 (half of the normal neostigmine dose), were given slowly to antagonize the neuromuscular block, and the trachea extubated. In both cases, anaesthetic management was uneventful, and no abnormality was detected on the ECGs. During the 24 h postoperative period in the intensive care unit, the patients recovered successfully without any worsening of ST segment elevation on the 12-lead ECG.
Careful preoperative evaluation and anaesthetic management is essential to avoid inducing arrhythmia. The high-risk criteria for patients with Brugada syndrome requiring general anaesthesia are:3 4 (i) symptomatic cases with syncope or a medical history of VF; (ii) asymptomatic cases showing pathognomonic ST segment elevation on ECG and medication- or EPS-induced VF; and (iii) cases showing coved-type ST elevation on ECGs.
The mechanism of ST-segment elevation with Brugada syndrome is associated with an imbalance in action potential gradients between the right ventricular endocardial and epicardial cells.2 Many factors during anaesthesia, in particular the autonomic nervous system, influence this imbalance.1 3–5 Postural change can be regarded as a factor and depth of anaesthesia should be sufficiently controlled before postural change, in order not to disturb autonomic nerve balance.
Neostigmine may augment ST segment elevation in a dose-dependent manner without inducing coronary spasm,1 3 5 while atropine may reduce elevation.1 3 Therefore, it may be wise to avoid neostigmine. However, in our cases, neostigmine doses were carefully divided and did not cause any abnormalities. There have been several reports of successful neostigmine administration without problems.1 5 We feel, neostigmine can be administered safely by careful dose adjustment and by atropine administration before neostigmine.
Most anaesthetics have inhibitory effects on circulation. However, specific differences and safety of the depressant action in each drug at clinical concentrations remain unknown. Further studies are required to clarify the safest anaesthetic management.
Yamaguchi, Japan
*E-mail: hayashida-myz{at}umin.ac.jp
References
1 Edge CJ, Blackman DJ, Gupta K, Sainsbury M. General anaesthesia in a patient with Brugada syndrome. Br J Anaesth 2002; 89:788–91
2 Tanaka H, Kinoshita O, Uchikawa S, et al. Successful prevention of recurrent ventricular fibrillation by intravenous isoproterenol in a patient with Brugada syndrome. Pacing Clin Electrophysiol 2001; 24:1293–4[CrossRef][Medline]
3 Kubo K, Nishikawa K, Goto F. Perioperative management of patients with Brugada syndrome. Masui 2005; 54:1247–52[Medline]
4 Santambrogio LG, Mencherini S, Fuardo M, Caramella F, Braschi A. The surgical patient with Brugada syndrome: a four-case clinical experience. Anesth Analg 2005; 100:1263–6
5 Inamura M, Okamoto H, Kuriowa M, Hoka S. General anesthesia for patients with Brugada syndrome. A report of six cases. Can J Anaesth 2005; 52:409–12
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