van der Heide et al. Journal of Medical Case Reports 2011, 5:368 http://www.jmedicalcasereports.com/content/5/1/368 such as b-blockers. Identification of the congenital LQTS genes uncovered groups of patients with normal resting ECGs. It is thought that these patients have an incomplete penetrance and that they are mutation car- riers or are carrying polymorphic congenital LQTS dis- ease genes. They are at risk of developing TdP when exposed to certain drugs [5]. Nothing, however, is known about adrenergic stimulation in this group of patients. An “epinephrine stress test” is sometimes per- formed to unmask this group of patients with a sup- posed congenital LQTS and a normal QT interval. In this provocative test, epinephrine is administered IV by bolus infusion (Shimizu protocol) or by incremental escalating infusion (Mayo protocol) while ECG changes are measured. A paradoxical response characterized by QT lengthening (rather than expected shortening) is seen more frequent in patients with LQT1 [9]. Our patient neither had a prolonged QT preopera- tively, nor was her family history suspect for a congeni- tal LQTS. Moreover, in a follow-up study, her exercise test and echocardiography results were also normal, and a 24-hour ambulatory monitoring only showed a short episode of a spontaneous supraventricular tachycardia, probably originated by atrial tachycardia. Possibly, she had a LQTS1 during surgery originated by excess of adrenergic stimulation. We did not perform genetic test- ing afterward to confirm this because noninvasive car- diac evaluation results were normal, and her family history results were negative. Most likely, our patient experienced an acquired LQTS. An acquired LQTS is predominantly elicited by drugs prolonging the ventricu- lar action potential or by an electrolyte imbalance [10]. In the present case, the combination of flecainide [10], hypomagnesaemia and adrenergic stimulation may have elicited increased transmural dispersion of repolariza- tion, resulting in TdP [6-8]. The increased adrenergic stimulation during manipulation of the tumor then likely resulted in premature ventricular beats either by abnormal automaticity or by early afterdepolarizations inducing a pause (long RR interval) and increased trans- mural dispersion of depolarization resulting in TdP. This is, however, easily said in a retrospective point of view. The choice of using flecainide was clear because there was atrial fibrillation, and the plasma magnesium level is not a standard preoperative measurement. Anesthetic guidelines on managing patients with pheochromocytoma stress the importance of preopera- tive treatment with a-blocking and, if necessary, with b- blocking agents. Often, phenoxybenzamine or doxazosin is advised [2,3,11]. Preoperative hemodynamic changes are preferably controlled with phentolamine, nitroprus- side and short-acting b-blockers such as esmolol [2,3,11]. Because no prospective, controlled, randomized trials have been performed on almost any aspect of the Page 4 of 5 diagnosis or treatment of pheochromocytoma, guidelines are based on expert opinions and case reports. TdP occurring in patients with pheochromocytoma is not expected, and specific combinations of drugs to mini- mize the risk of TdP are unknown. We advise, under- standably, that sufficient a- and b-blockade is mandatory, but QT-prolonging drugs should also be avoided [10]. Moreover, potassium and magnesium plasma levels should be kept at normal to high levels. Conclusion A laparoscopic adrenalectomy of a pheochromocytoma in a patient without preoperative QT interval prolonga- tion may result in TdP, most likely elicited by an excess of adrenergic stimulation. Thorough preoperative a- and b-blockade is advised, QT-prolonging drugs should be avoided and potassium and magnesium plasma levels should be kept at normal to high levels. Consent Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal. Acknowledgements Special regards to Dr. B.A. Schoonderwoerd, cardiologist at the University Medical Centre of Groningen, The Netherlands. Author details 1Department of Emergency Medicine, University Medical Centre Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands. 2Department of Anaesthesiology, Rijnstate Ziekenhuis, PO Box 9555, 6800 TA Arnhem, The Netherlands. 3Department of Anaesthesiology, University Medical Centre Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands. 4Department of Cardiology, University Medical Centre Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands. Authors’ contributions KvdH, AdH and HGDH were present during the event described in this case report. KvdH and AdH collected the literature and the patient data. KvdH was the major contributor in writing the manuscript. Reviewing the manuscript was mostly done by KvdH, JKGW and HGDH. ACPW was asked for her expertise on torsades de pointes and also contributed to reviewing the manuscript. All authors read and approved the final manuscript. Competing interests The authors declare that they have no competing interests. Received: 23 November 2010 Accepted: 12 August 2011 Published: 12 August 2011 References 1. Lenders JW, Eisenhofer G, Mannelli M, Pacak K: Phaeochromocytoma. Lancet 2005, 366:665-675. 2. Prys-Roberts C: Phaeochromocytoma–recent progress in its management. Br J Anaesth 2000, 85:44-57. 3. Fleisher LA: Diseases of the endocrine system. In Anaesthesia in Uncommon Diseases.. 5 edition. Edited by: Fleisher LA. St. Louis: Saunders Elsevier; 2006:440-443. 4. Gowda RM, Khan IA, Wilbur SL, Vasavada BC, Sacchi TJ: Torsade de pointes: the clinical considerations. Int J Cardiol 2004, 96:1-6.