Electrosurgical units (ESU) are very safe. The typical ESU for general surgery is monopolar. The active handpiece is this single pole. The circuit is completed by a dispersive electrode placed on a well-insulated part of the patient. It is at the tip of the handpiece only that the current density is great enough to cause tissue damage. The voltages applied run from thousands to tens of thousands of volts. The power settings vary from tens to hundreds of watts [1,2]. The response to an electrical current flow through the body depends on the amplitude and frequency of the current. Small currents over large areas have less impact than the same current over a smaller area. The myocardium is most sensitive to 30-100 Hz electricity, so electrical power generation at 50 Hz or even 60 Hz is ideal for inducing fibrillation. Higher frequencies (i.e. surgical diathermy) and alternating current, which does not pass through the heart, do not cause fibrillation but rather heat up and burn the muscle. If direct current or high-frequency alternating current passes through the body, heating effects and ultimately burns will occur . It is this effect that is intentionally created when electrosurgical generators are used to cut tissue and coagulate fluids. If low-frequency alternating current is applied to the body, muscular polarization and depolarization take place that can ultimately create a ‘circus movement’ in the heart muscle, resulting in fibrillation and death .
In the operating room, electrocution hazards are described as macroshock and microshock . Macroshock refers to the application of large voltage or currents to the tissue. Microshock refers to the application of low-voltage and low-frequency current directly to the heart . Microshock electrocution can cause ventricular fibrillation with voltages as low as 0.05 V.
We report a case of electrical injury during electrocautery leading to recurrent spontaneously reversible asystole.
A 60-yr-old male was scheduled for a left pneumonectomy. Preoperative physical examination and preoperative 12-lead electrocardiograph (ECG) were normal. A titanium central venous access (porth-a-cath, Celsite-ST 301, Braun, USA) was implanted 2 weeks before lung surgery to facilitate preoperative intravenous (i.v.) chemotherapy. Chest X-ray showed the reservoir under the right clavicle and the extremity of the catheter located at the junction of the superior vena cava and the right atrium.
Monitoring included an ECG (leads II, VR and V5), pulse oximeter, capnograph and invasive blood pressure (BP) monitor (AS3, Datex Cie, Helsinki, Finland). Induction of anaesthesia and tracheal intubation using a double-lumen tube were uneventful, maintenance of anaesthesia was with isoflurane and i.v. sufentanil.
The patient developed brief asystole during intercostal muscular dissection, but the cardiac rhythm returned to normal after a few seconds. However the asystole resumed a few minutes later and we realized that it was concomitant with the use of the ESU (Lamidey, intersurgical 4000, France). We asked the surgeon to use the electrocautery once more, and the sequence of the accident was as follows: the surgeon commanded the electrosurgery unit in the coagulation mode using a soft pedal, asystole occurred, then he applied the tip of the electrosurgical knife to the tissue inside the thorax and electrical artefact appeared on the ECG. The third event was registered on the monitor (Fig. 1). Trace A shows the recorded ECG (standard lead II) showing a transient period of asystole due to sinus arrest followed by the artefact due to electrocautery, Trace B the concomitant recorded radial artery pressure which was absent during the period of asystole, confirming the absence of perfusion.
We stopped surgery and examined the equipment for malfunction. The electrocauterization dispersive plate appeared normal and correctly placed. However, the plate and the ESU were changed for further technical verification and the surgeon was asked to use bipolar electrocautery. Surgery was resumed uneventfully. The patient's electrocardiogram was monitored overnight and repeated electrocardiograms were normal. Creatinine phosphokinase and troponin Ic levels were 557 UI L−1 and 0.42 μg L−1, respectively at the end of surgery; troponin Ic levels were 0.62 μg L−1 5 h later and 0.05 μg L−1 the following day (institution reference range for normal troponin level is <0.8 μg L−1).
Technical investigation was conducted; electric isolation of the operating room, the electrocautery unit and electrical dispersive pad attached to the patient were tested. It was concluded that the electrical environment of the room was operating correctly and within accepted guidelines. The electrocautery unit had been tested 5 months before and was normal (i.e. alarms, level of high-frequency currents and level of leak current were tested and normal).
The link between the asystole and the use of the ESU is not in doubt because of the reproducibility of the accident. Asystole occurred three times and the reiteration of the phenomenon was exactly the same each time: command of the ESU by the soft pedal, asystole then contact of the tip of the electrosurgical knife and electrical artefact on the ECG.
The mechanism involved in the case report remains putative either low-voltage and low-frequency leakage current (i.e. microshock) or low-voltage radio-frequency leakage current (i.e. radio-frequency burn) [1,2].
The mechanism of microshock is complex, due to direct leakage currents flowing through defects in active electrode insulation or capacitive stray currents originating from the shaft of the active electrode. If electrical contact is made internally, especially on or close to the heart, very low currents, as low as 10 mA, may initiate dysrhythmia. The resistance of skin contact is eliminated and the current density at the interface between the contact and the heart is very high. Normally skin resistance is quite high and this is a safety barrier to electrocution. In thoracic surgery, this skin barrier is lost and microshock may occur, but the risk is much more common when conductive saline is used as the fluid in a cardiac catheter, a pulmonary artery catheter or a central venous pressure (CVP) catheter . Ventricular dysrhythmias due to electrical microshock have been recognized in several patients undergoing cardiac catheterization or connected to electronic equipment instruments . The role of the central venous line as a vector of leakage current is supported by experimental study and clinical observations. Monies-Chass and colleagues  showed on dogs catheterized for the measurement of CVP, with the catheter advanced into the right ventricle, that currents less than 500 mA caused interference with heart rhythm. As ventricular fibrillation in human hearts is alleged to require a minimum of 50 mA, the accepted guidelines sets 10 mA as the maximum permissible leakage current allowed through electrodes or catheters that contact the heart. In this case we report, the injury was not ventricular fibrillation but asystole, collapse and cardio-circulatory arrest which were spontaneously reversible. Nevertheless, the link between 60 Hz intracardiac leakage current and cardiovascular collapse have been demonstrated by Swerdlow and colleagues . In patients with intracardiac electrodes, stimulation by silent alternating current below the ventricular fibrillation threshold, which is neither felt nor visible on the ECG presents as hypotensive ventricular tachycardia. But as far as we know, microshock induced ventricular fibrillation and not asystole as we report.
Other hypothetical mechanisms include electrical burns caused by ESU leakage current, stray current resulting from insulation failure, direct coupling of the ESU to other surgical instruments or capacitive coupling of the ESU signal due to the nature of radio-frequency transmission . The radio-frequency leakage current hypothesis is sustained by Schlapfer and colleagues  describe a case of asystole induced by a low-voltage radio-frequency application to the coronary sinus to treat an accessory pathway. This is a Bezold-Jarisch-like phenomenon, which is an inhibitory reflex originating in sensory receptors with vagal afferents. This reflex produces an increase in parasympathetic activity resulting in bradycardia, vasodilatation and hypotension. The problem is that we cannot explain how a very high-frequency current was generated in the patient. Nevertheless, the fact that ESU activation produced asystole prior to application of the ESU to the patient argues strongly for radio-frequency induced current entering the heart via the antenna that was present in the patient - the titanium central line. Other causes of transient asystole during thoracic surgery may be discussed, such as a sick sinus syndrome induced by anaesthesia medications but these were very improbable, because of the reproducibility of the event.
In conclusion, we describe the case of a patient who experienced an electric accident during thoracic surgery, which induced reversible cardio-circulatory arrest. We assume that a low-voltage leakage current was conducted via the central venous line to vagal afferent fibres located at the junction of the vena cava and the atrium. This resulted in powerful electric stimulation and to vagal overactivity, and finally to transient asystole. Patients with an indwelling catheter are susceptible to microshock electrocution and are designated as electrically vulnerable patients.
*Department of Anaesthesiology, Foch Hospital, Suresnes, France
†Department of Thoracic Surgery, Foch Hospital, Suresnes, France
¶Department of Cardiology, Parly II CMC, Le Chesnay, France
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