External Cardiac Defibrillation Does Not Cause Acute Histopathological Changes Typical of Thermal Injuries in Pigs with In Situ Cerebral Stimulation Electrodes Christian Kolbitsch, MD, DEAA*, Wilhelm Eisner, MD†, Axel Kleinsasser, MD*, Matthias Biebl, MD‡, Thomas Fiegele, PhD†, Alexander Lo ¨ ckinger, MD*, Ingo H. Lorenz, MD*, Gregor Mikuz, MD, FRCPath§, and Patrizia L. Moser, MD§ Departments of *Anaesthesia and Intensive Care Medicine, †Neurosurgery, ‡Vascular Surgery, and §Pathology, University of Innsbruck, Austria Parkinson’s disease patients with long-term l-dopa syndrome may benefit from an implanted cerebral stimulation device. When advanced life support de- mands cardioversion or defibrillation in these patients, undesired effects of monophasic electroshocks might occur in brain tissue adjacent to the stimulation elec- trodes (e.g., thermal injury), but also in the stimulation device itself. Thus, in this animal study (n = 6 pigs), we investigated the effects of repeated defibrillation (2  200 J [n = 1] and 2  360 J [n = 5]) at the implantation site of cerebral stimulation electrodes and on stimulation device function. Repeated external cardiac defibrilla- tion did not cause acute histopathologic changes typical of thermal injury to brain tissue adjacent to the cerebral stimulation electrodes. Functionality of the stimulator device after defibrillation, however, ranged from nor- mal to total loss of function. Therefore, when defibrilla- tion is performed, the greatest possible distance be- tween the defibrillation site and the stimulator device implantation site should be considered. Subsequent test- ing of the stimulator device’s function is mandatory. (Anesth Analg 2004;98:458 –60) T herapeutic implantation of stimulation elec- trodes to various brain structures has become an established neurosurgical intervention in pa- tients with advanced Parkinson’s disease (PD) with motor complications of l-dopa long-term therapy (1– 6). An increasing number of PD patients subsequently present with such a cerebral stimulation device in situ in daily routine, but also in the case of cardiac emer- gency. Because cardiac emergency often calls for ex- ternal cardioversion, as well as defibrillation (7–9), defibrillation on brain tissue adjacent to the stimula- tion electrodes (e.g., thermal injury), and also on the stimulation device itself, might cause undesired ef- fects. This animal study thus investigated the effects of repeated defibrillation on brain tissue at the implan- tation site of cerebral stimulation electrodes and on stimulation device functionality. Methods The study was approved by the Austrian Federal Ani- mal Investigation Committee, and pigs (German/ Pietrain; n = 6; 16 wk old; 40 kg) were managed in accordance with the National Institutes of Health and the Utstein style guidelines (10). Animals were fasted overnight but had free access to water. Pigs were pre- medicated with azaperone (4 mg/kg IM) and atropine (0.01 mg/kg IM) 1 h before surgery. After the induction of anesthesia with ketamine (20 mg/kg IM) and propo- fol (2– 4 mg/kg IV), the trachea was intubated, and the lungs were mechanically ventilated (fraction of inspired oxygen, 0.4; end-tidal carbon dioxide concentration, 40 mm Hg). Anesthesia was maintained with propofol (6 – 8 mg · kg -1 ·h -1 ) and boluses of piritramide (30 – 45 mg). Lactated Ringer’s solution (10 mL · kg -1 ·h -1 ) was administered throughout the experiment. Depth of anesthesia was adjusted according to blood pressure and heart rate. No paralyzing drug was used. Body temper- ature was maintained at normothermia (38°C–39°C) by means of heating blanket. Monitoring included a standard lead II electrocar- diogram (ECG) and invasive blood pressure meas- urement in the femoral artery (diameter, 1.2 mm; Accepted for publication August 26, 2003. Address correspondence and reprint requests to C. Kolbitsch, MD, Department of Anesthesia and Intensive Care Medicine, University of Innsbruck, Anichstr. 35, A-6020 Innsbruck, Austria. Address e-mail to christian.kolbitsch@uibk.ac.at. DOI: 10.1213/01.ANE.0000096192.33388.48 ©2004 by the International Anesthesia Research Society 458 Anesth Analg 2004;98:458–60 0003-2999/04