Sir,Pheochromocytoma is catecholamine secreting tumor from the chromaffin cells of adrenal and extra adrenal sites. The most interesting thing is the variation in its presentation from an incidental finding to classic triad of episodic head ache, sweating, and tachycardia leading to episodic hypertension.[1] Moreover, the undiagnosed pheochromocytoma presented for incidental surgery, induction of anesthesia may precipitate a hypertensive crisis. In this situation, mortality may be up to 80%.[2]A 20-year-old married female, weighing 42 kg, was presented with the complaint of amenorrhea for 2 months. On evaluation, urine for pregnancy test negative, and the lady had deranged blood sugar levels and hypertension. Subsequently, she was diagnosed to be a case of catecholamine secreting tumor on the basis of computed tomography scan, positron emission tomography scan serum, and urine catecholamine levels.Computed tomography abdomen revealed bilateral suprarenal gland tumor; right one was larger, 4 cm in largest dimension and the left one was 2 cm. Her plasma and urinary catecholamine's level confirmed the diagnosis of pheochromocytoma and the tumor was found to be a noradrenaline secreting one. Initially tablet prazosin was started and after 10 days, when hematocrit value started to come down, tablet metoprolol was also added. A two-dimensional and M-mode echocardiography revealed concentric left ventricular hypertrophy, grade I diastolic dysfunction, and ejection fraction of 60%.She was planned for bilateral excision of tumor when a predetermined criterion for control of catecholamine excess has been achieved. Her fasting blood sugar, urine sugar and ketones, serum electrolytes were within normal limit on the morning of surgery. Surgery was scheduled at 10 a.m. and last dose of prazosin was administered at 5 a.m. She was premedicated with tablet diazepam 5 mg and pantoprazole 40 mg on the night before surgery and on the morning of surgery. Pre-induction left radial artery was cannulated with a 20 gauge arterial cannula. Anesthesia was induced with intravenous fentanyl 150 µg and propofol 120 mg and muscle relaxation was achieved by vecuronium 6 mg. Intravenous labetalol 20 mg was given to blunt sympathetic responses of laryngoscopy and intubation. Hemodynamic changes during intubation were insignificant. After induction of general anesthesia a 7.5 Fr triple lumen central venous catheter was inserted in right internal jugular vein with the help of real time ultrasound guidance.Anesthesia was maintained with oxygen-nitrous oxide-isoflurane with targeting an end-tidal concentration of 0.8–1.0 minimum alveolar concentration of inhalation anesthetic.Immediate preoperative blood sugar was found to be 241 mg/dL and insulin infusion of 2 U/h and 5% dextrose - 09% saline - 20 mEq/L KCl was started at maintenance rate. Hourly blood glucose monitoring was initiated and insulin infusion adjusted accordingly targeting a blood glucose value <200 mg/dL.Intraoperative hemodynamic changes due to sympathetic stimulations, that is, hypertension and tachycardia were managed by boluses of esmolol and infusion of sodium nitroprusside. Severity of hemodynamic changes decreased significantly during handling of the left tumor in comparison to the right one and blood sugar also started to decrease after removal of the right one. Just after removal of the left tumor, blood pressure started to fall and infusion noradrenaline was started to maintain a mean arterial pressure >70 mm Hg. At the end of surgery, inhalation anesthetic was stopped, residual neuromuscular block was reversed with neostigmine and glycopyrrolate and patient was extubated when fully awake and shifted to Intensive Care Unit (ICU) for further management. In the ICU, infusion noradrenaline was continued and a patient controlled analgesia morphine was also started. Infusion noradrenaline was gradually tapered and weaned of in the next 24 h. Rest of her postoperative course was uneventful. Arterial blood pressure monitoring was continued 2 h after weaning from noradrenaline.Bilateral pheochromocytoma is the relatively uncommon condition, and one of the two tumors may be smaller and nonfunctioning.[3] A bilateral adrenal tumor may be a pheochromocytoma with an adrenal adenoma also.[4]In our case, the diagnosis of pheochromocytoma was made after quite a long time as she presented as secondary amenorrhea and type I diabetes mellitus (DM). Pheochromocytoma may have different clinical presentations, according to the amount and type of catecholamine secreted and number and biological activity of co-secreted peptides. The association of pheochromocytoma with other endocrinopathies is a rare yet recognized phenomenon. Previous studies have concluded that DM is present in up to a third of patients presenting with pheochromocytoma.[567] This encompasses type I, type II, and gestational DM. Catecholamine over production leads to both decreased insulin secretion and increased peripheral resistance to insulin action, by stimulating α2 and β2 adrenoceptors, respectively. Following adrenalectomy, some patients revert to normoglycemia with a normal glucose tolerance test, yet a proportion of patients continue to display features of glucose intolerance.[56] Recent literature has also reported a rare association of autoimmune hypo- and hyperthyroidism with pheochromocytoma.[8] Thus, a high index of suspicion for pheochromocytoma should be maintained in the context of concomitant endocrinopathies and typical or atypical symptomatology. An undiagnosed pheochromocytoma may be of devastating consequences during surgery and anesthesia, so a high index of suspicion is required. Again, one of such bilateral tumor may be nonfunctioning or less functioning also, so timely institution of vasopressor/inotropes therapy in such cases is of paramount importance.