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Year : 2012  |  Volume : 6  |  Issue : 1  |  Page : 101-104  

Anaesthetic management of a patient of Brugada syndrome for an emergency appendicectomy

Department of Anaesthesia, SICU, TICU, Hamad Medical Corporation, Doha, State of Qatar

Date of Web Publication14-Nov-2012

Correspondence Address:
Chetankumar Raval
Department of Anaesthesia, SICU, TICU, Hamad Medical Corporation, PO Box: 3050, Doha
State of Qatar
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0259-1162.103390

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Brugada syndrome is a myocardial transmembrane conduction of sodium abnormality and a common cause of sudden cardiac death. It is characterized by a distinctive electrocardiograph pattern with right bundle branch block and ST segment elevation in precordial leads V 1 -V 3 . Many factors during general anesthetic management could precipitate malignant dysrhythmia. We report the anesthetic management of a patient with Brugada syndrome for emergency appendectomy uneventfully.

Keywords: Aanesthetic management, Brugada syndrome, emergency appendicectomy

How to cite this article:
Raval C, Saeed K. Anaesthetic management of a patient of Brugada syndrome for an emergency appendicectomy. Anesth Essays Res 2012;6:101-4

How to cite this URL:
Raval C, Saeed K. Anaesthetic management of a patient of Brugada syndrome for an emergency appendicectomy. Anesth Essays Res [serial online] 2012 [cited 2022 Dec 6];6:101-4. Available from:

   Introduction Top

In 1992, Brugada and Brugada [1] described this syndrome. This syndrome is associated with a significant risk of ventricular tachyarrhythmias (Ventricular Fibrillation) and sudden death. Eight patients presented with RBBB and St Segment elevation in leads V 1 -V 3 without any demonstrable structural heart disease were resuscitated from cardiac arrest. It is especially seen in Asian populations. [2] The syndrome is familial with an autosomal dominant mode of transmission and incomplete penetrance. Arrhythmic events are observed at an average age of approximately 40 year, but have been reported over a wide range of ages from 2 to 77 year. [3] Many factors during general anesthesia (medications, bradycardia, and temperature changes) could precipitate malignant dysrhythmia. To date, a few case series and case reports of general anesthesia in Brugada syndrome have been published. We herewith report a patient with Brugada syndrome for emergency appendicectomy under general anesthesia.

   Case Report Top

A 45-year-old male patient Asian origin (-Kerala, India) was admitted with pain in abdomen, nausea, and vomiting with fever since 2 days. Clinical symptoms, signs, and investigations were suggestive of acute appendicitis. Patient was scheduled for an emergency appendicectomy. His weight and height were 70 kg and 173.5 cm, respectively with BMI 23.25. On medical history he had chest pain and for the same was admitted to Hamad general Hospital 1 year back. There was no history of chest pain after that episode, syncope, palpitations in the past. He was investigated with normal blood investigations during that time. But on ECG there was RBBB with ST elevation (coved) in lead V 1 -V 3 . Holtermonitorings were done suggestive of atrial premature contractions. On the stress test, as per Bruce protocol, it was negative with the target rate, no ECG abnormality. So cardiologist suggested that baseline ECG suggestive of Brugada syndrome. He was having past history of productive cough, which was diagnosed as asthmatic bronchitis 3 weeks back. He received antibiotics and salbutamol inhaler (as and when required- last used 3 weeks back). There was family history of father's sudden death, but details are not available. No past surgical or allergic history. On general and airway examination was normal except fever. Systemic examination was normal except abdominal tenderness. Chest X-ray was normal. ECG findings same as before RBBB with ST elevation (coved) in lead V 1 -V 3 with QTc 420 msec.

Looking at clinical examination, investigations and as per surgical indication, general anesthesia with avoidance of sodium channel blocker medications was planned. Detail explanation given to patient and consent was taken. Routine monitorings were used. Defibrillator was kept ready. Atropine as per routine was kept ready for abolish any vagal effect. As any vagal stimulation in this type of cases, this leads to dysrrthymias.

General anesthesia was induced with propofol 2.5 mg/ kg and neuromuscular blockade provided through atracurium 0.5 mg/kg. Analgesia was supplemented with fentanyl 2 mcg/kg and patient maintained on sevoflurane with air for controlled ventilation. Paracetamol 1 gm intravenous was given. Spontaneous extubation was carried out with smooth emergence and breathing spontaneously, obeying commands, and satisfactory muscle power. Neostigmine was avoided due to its ability to produce dysrthymia in these cases. Postoperative analgesia provided with morphine in titrated doses. Postoperative care was given in the postanaesthesia care unit. No untoward events (no bradycardia or ventricular fibrillation) occurred during the anesthesia. Total surgery and anaesthesia times were 45 and 65 min, respectively. Invasive monitorings were avoided due to short surgical procedure without much haemodynamic instability. Patient was discharged following an uneventful hospital stay.

   Discussion Top

Brugada syndrome is characterized by abnormal electrocardiogram findings and is also known as sudden unexpected death syndrome or sudden unexpected nocturnal death syndrome.

An estimated 4% of all sudden deaths and at least 20% of sudden deaths in patients with structurally normal hearts are due to the Brugada syndrome. [1],[2],[3],[4] Brugada syndrome is genetically linked with mutation of alpha subunits of tetrodotoxin-"insensitive" human cardiac sodium channels (hH1) gene SCN5A. [5] The use of certain antiarrhythmic sodium channel blockers (class IA and IC) accentuate the ECG manifestations. [6]

The following criteria were used to diagnose Brugada syndrome: [7] [1] history of cardiac arrest or aborted sudden death or syncope of unknown origin with or without documentation of VF; [2] ST segment elevation (coved or saddleback type) in V 1 -V 3 with or without a certain degree of right bundle branch block (RBBB); [3] no prolongation of the QT interval (QTc<440 msec); [4] no structural and ischemic heart disease demonstrated by echocardiography and cardiac catheterization. In about 20% of the patients, atrial fibrillation is an associated arrhythmia. [8]

According to above favouring criteria, in our patient had ST segment elevation (coved or saddleback type) in V 1 -V 2 with RBBB. There was no prolongation of QTc (420 msec) in ECG [Figure 1]. There was no structural heart disease and stress test negative as per Bruce protocol. He was having history of chest pain 1 year back but no syncope investigated for the same and Halter monitoring was done showed atrial premature contractions. There was family history of father's sudden death but no detail found. As surgery was an emergency, other diagnostic tests were not feasible.
Figure 1: ECG of our patient of Brugada syndrome

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Type 1 has a coved-type ST elevation with at least 2-mm J-point elevation, a gradually descending ST segment and a negative T-wave [Figure 2]. The electrocardiogram picture in this study shows the typical Type 1 pattern. Type 2 has a saddle back pattern with a least 2-mm J-point elevation and at least 1-mm ST elevation, with a positive or biphasic T-wave. The type 2 pattern can occasionally be seen in healthy subjects. Type 3 has a saddle-back pattern with <2-mm J-point elevation and <1-mm ST elevation, with a positive T-wave. Type 3 pattern is not uncommon in healthy subjects. [9]
Figure 2: Typical ECG types of Brugada syndrome

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Drug challenge with sodium channel blockers such as Pilsicainide and Flacainide is a standard provocative test used to unmask Brugada syndrome. It can induce significant ST segment elevation>0.10 mV. Test has high sensitivity (92%) and specificity (89%) for detection of programmed electrical stimulation (PES) - induced ventricular fibrillation in asymptomatic patients is till controversial. [10]

Fever, vagal stimulation, administration of class Ia, Ic, and III drugs and neostigmine also accentuate the ST segment elevation. [11] So in our patient we have not used neostigmine. Volatile anesthetic has no effect on ECG [Table 1]. Local anesthetics, especially bupivacaine, given by any route (eg. epidural), which cause a sudden rise in the serum concentration can unmask Brugada syndrome. [12] Lignocaine, a class IIb antiarrhythmic drug has no such effect and can be safely used. [13] Acetylcholine, beta antagonists and nicorandil may interfere with the ionic conditions and exacerbate the manifestations. Neostigmine may augment ST-segment elevation in a dose-dependent manner without inducing coronary spasm, while atropine may reduce elevation. Therefore, it may be wise to avoid neostigmine. [14]
Table 1: Acceptable and contraindicated drugs for Brugada syndrome[15],[16]

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To date; an implantable cardioverter-defibrillator (ICD) is the sole medical intervention that effectively protects patients with Brugada syndrome from sudden cardiac death. [15],[16]

   Conclusion Top

Vigilance on examination of ECG is required, as RBBB is very common and with normal cardiac function in 10% of patient may nearly miss diagnosis of this syndrome. Such patients are often untreated, but they have the risks of cardiac accidents such as ventricular fibrillation or sudden death. For preoperative evaluation of patients with Brugada syndrome-like ECG, it is important to ask them their experience of syncope and family history. Echocardiography and Holter ECG recording should be done. External defibrillator should be prepared and parasympathetic dominant condition must be avoided during the anesthetic management.

Timely detection of cardiac arrhythmias and immediate treatment is very important. By avoiding agents or conditions that may exacerbate Brugada syndrome during anesthesia, we were able to manage our patient uneventfully.

   References Top

1.Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: A distinct clinical and electrocardiographic syndrome. J Am Coll Cardiol 1992;20:1391-6.  Back to cited text no. 1
2.Alings M, Wilde A. "Brugada" syndrome. Clinical data and suggested pathophysiological mechanism. Circulation 1999;99:666-73.  Back to cited text no. 2
3.Priori SG, Napolitano C, Giordano U, Collisani G, Memmi M. Brugada syndrome and sudden cardiac death in children. Lancet 2000;355:808-9.  Back to cited text no. 3
4.Antzelevitch C, Brugada P, Borggrefe M, Brugada J, Brugada R, Corrado D, et al. Brugada syndrome: Report of the second consensus conference: Endorsed by the Heart Rhythm Society and the European Heart Rhythm Association. Circulation 2005;111:659-70.  Back to cited text no. 4
5.Rook MB, Bezzina Alshinawi C, Groenewegen WA, van Gelder IC, van Ginneken AC, Jongsma HJ, et al. Human SCN5A gene mutations alter cardiac sodium channel kinetics and are associated with the Brugada syndrome. Cardiovasc Res 1999;44:507-17.  Back to cited text no. 5
6.Brugada R, Brugada J, Antzeledvitch C, Kirsch GE, Potenza D, Towbin JA, et al. Sodium channel blockers identify risk for sudden death in patients with ST-segment elevation and right bundle branch block but structurally normal hearts. Circulation 2000;101:510-5.  Back to cited text no. 6
7.Wilde A, Antzelevitch C, Borggrefe M, Brugada J, Brugada R, Brugada P,et al. Proposed diagnostic criteria for the Brugada syndrome. Consensus report. Study Group on the Molecular Basis of Arrhythmias of the European Society of Cardiology. Circulation 2002;106:2514-9.  Back to cited text no. 7
8.Bordachar P, Reuter S, Garrigue S, Caï X, Hocini M, Jaïs P, et al. Incidence, clinical implications and prognosis of atrial arrhythmias in Brugada syndrome. Eur Heart J 2004;25:879-84.  Back to cited text no. 8
9.Goraksha S, Bidaye S, Gajendragadkar S, Bapat J, Butani M. General anaesthesia for insertion of an automated implantable cardioverter defibrillator in a child with Brugada and autism. Indian J Anaesth 2010;54:562-4.  Back to cited text no. 9
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10.Morita H, Takenaka-Morita S, Fukushima-Kusano K, Kobayashi M, Nagase S, Kakishita M, et al. Risk stratification for asymptomatic patients with Brugada syndrome. Circulation J 2003;67:312-6.  Back to cited text no. 10
11.Edge CJ, Blackman DJ, Gupta K, Sainsbury M. General anaesthesia in a patient with Brugada syndrome. Br J Anaesth 2002;89:788-91.  Back to cited text no. 11
12.Phillips N, Priestly M, Denniss AR, Uther JB. Brugada type electrocardiographic pattern induced by epidural bupivacaine. Anesth Analg 2003;97:264-7.  Back to cited text no. 12
13.Miyazaki T, Mitamura H, Miyoshi S, Soejima K, Aizawa Y, Ogawa S. Autonomic and antiarrythmic drug modulation of ST segment elevation in patients with Brugada Syndrome. J Am Coll Cardiol 1996;27:1061-70.  Back to cited text no. 13
14.Hayashida H, Miyauchi Y. Anaesthetic management in patients with high-risk Brugada syndrome Br J Anaesth2006;97:118-9.  Back to cited text no. 14
15.Inamura M, Okamoto H, Kuroiwa M, Hoka S. General anesthesia for patients with Brugada syndrome - A report of six cases. Can J Anesth 2005;52:409-12.  Back to cited text no. 15
16.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.  Back to cited text no. 16


  [Figure 1], [Figure 2]

  [Table 1]

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