van der Heide et al. Journal of Medical Case Reports 2011, 5:368 http://www.jmedicalcasereports.com/content/5/1/368 norepinephrine in a lesser degree). For symptomatic treatment, combined a- and b-blockade was started with doxazosin (8 mg once daily per os [PO]) and pro- pranolol (20 mg thrice daily PO). Because electrocardio- graphy showed atrial fibrillation, the patient was also treated with flecainide (100 mg once daily PO) and ace- nocoumarol (PO; INR conducted, 2.5-3.5). Preoperative examination revealed a blood pressure of 130/75 mm Hg in the supine position (120/85 mm Hg standing upright) under combined a- and b-blockade. At admission, she had a sinus bradycardia of 58 beats/ min with a normal QRS width (110 msec) without pro- longed corrected QT interval (QTinterval corrected for heart rate (QTc), 435 msec) (Figure 1a). Blood count and serum electrolytes were within nor- mal ranges, but her serum magnesium level was not determined. Anesthesia was performed with propofol (2.5 mg/kg intravenously [IV]), sufentanil (0.4 μg/kg IV) and rocur- onium (0.6 mg/kg IV). Isoflurane (1.1%-1.3%) was used for maintenance along with increments of sufentanil and rocuronium when appropriate. A central venous line (16-Fr, double-lumen, right internal jugular vein), an arterial line (20 gauge; left radial artery) and two periph- eral IV lines (14 and 20 gauge) were inserted. To per- form a left laparoscopic adrenalectomy, the patient was placed in a right lateral position. The patient’s blood pressure and heart rate remained stable during induc- tion and positioning. Immediately after surgical manipulation of the tumor, the patient’s blood pressure increased from 155/95 to 200/105 mm Hg. To control hypertension, nitroprusside (25 μg/kg/hr IV) was started, and an extra propofol bolus (100 mg IV) was administered. Despite these mea- sures, the second surgical manipulation of the tumor resulted in a blood pressure of 245/110 mm Hg immedi- ately followed TdP (Figure 1b). On request of the anesthetist, the surgeons stopped manipulating the tumor, resulting in a spontaneous return toward sinus rhythm within a few seconds and a gradually normaliz- ing of the blood pressure. However, each time the sur- geons tried to ligate the tumors venous return, the blood pressure elevated. Nitroprusside was increased to 130 μg/kg/hr, and two esmolol boluses of 20 mg each were administered. Also, anesthesia was deepened with propofol (100 mg thrice) and two sufentanil boluses of 20 μg and 10 μg. Despite these interventions, the patient’s blood pressure did not decrease below diastolic blood pressure of 105 mm Hg. At each blood pressure peak (maximum, 254/112 mm Hg), the patient showed TdP. In total, she experienced this arrhythmia four times, all returning to sinus rhythm. The total period of arrhythmias lasted 15 minutes and ended abruptly when the venous return of the tumor was Page 2 of 5 ligated. Subsequently, the tumor was successfully removed. Serum electrolytes were tested directly after removal of the tumor and revealed slight hypomagnesae- mia (0.54 mmol/L), normokalemia and normal sodium. Pupillary reflexes were found normal during the whole procedure. To prevent hypotension after tumor ligation, the patient was administered IV norepinephrine (10 mg/ 50 mL), which could be stopped at the end of the opera- tion. The postoperative electrocardiogram (ECG) showed sinus rhythm with 77 beats/min, but in contrast to the preoperative ECG, now with prolonged QT interval (QTc 505 msec) and U waves (Figure 1c). Her postoperative stay was uneventful. Pathologic examination confirmed the diagnosis of a pheochromocytoma. Discussion We describe the case of a patient without QT prolonga- tion preoperatively with recurrent TdP during laparo- scopic removal of a pheochromocytoma. TdP is a form of polymorphic ventricular tachycardia, predominantly occurring in the setting of a prolonged QT interval, T- wave abnormality or increased U-wave amplitude [4]. It occurs frequently in the presence of severe bradycardia and often precedes ventricular fibrillation. Electrocardio- graphically, TdP is a pattern of continuously changing morphology of the QRS complexes twisting around an imaginary baseline. In most cases, including in our patient, TdP is preceded by a characteristic sequence of a long RR interval followed by a short extrasystolic interval with premature depolarization interrupting the preceding repolarization, called the short-long-short phenomenon (Figure 1b). The QT interval represents the depolarization and repolarization of the ventricles [5-8]. Prolongation of the QT interval is caused by an increase in action potential duration of ventricular myocytes [6-8]. The ventricular myocardium is predominantly composed of three cell types that are histologically alike yet vary electrophysio- logically and pharmacologically. These three cell types may respond differently to drug- or disease-mediated action potential prolongation and hence differences in repolarization ("inhomogeneous prolongation of repolar- ization”). Transmural dispersion of repolarization may occur [7], which may be considered the electrophysiolo- gic cause of TdP. Transmural dispersion of repolariza- tion may be increased by an adrenergic agent such as isoproterenol [6-8]. In contrast to the patient’s normal preoperative QT interval, the postoperative QT interval was prolonged. A QT interval can be prolonged congenitally or acquired. Congenital long QT syndrome (LQTS) is subdivided into 10 genotypes. In LQT1 and LQT2, cardiac events may be precipitated by physical or emotional stress. These patients are treated with antiadrenergic therapy,