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Phaeochromocytoma Crisis: Two Cases of Undiagnosed Phaeochromocytoma Presenting after Elective Nonrelated Surgical Procedures

DOI: 10.1155/2013/514714

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Abstract:

Phaeochromocytoma is a catecholamine producing tumour and an uncommon cause of hypertension. We present two cases of relatively asymptomatic individuals, in which previously undiagnosed phaeochromocytoma was unmasked by elective nonadrenal surgical procedures, manifesting as postoperative hypertensive crisis and subsequent cardiogenic shock. The initial management in intensive care is discussed, in addition to the clinical and biochemical diagnostic challenges present. Successful adrenalectomy was performed in each case. 1. Introduction Phaeochromocytomas are rare catecholamine secreting tumours arising from chromaffin cells of the adrenal medulla and extra adrenal paragangliomas [1]. Secretion of catecholamines in phaeochromocytoma can be episodic or biochemically silent and therefore can present difficulty in diagnosis; however, failure to diagnose phaeochromocytoma can have fatal consequences. Classic symptoms include headache, palpitations, sweats, and sustained or paroxysmal hypertension, as a result of elevated catecholamine production [2]; however, presentation can be varied. A “hypertensive crisis” as the initial manifestation of undiagnosed phaeochromocytoma is rare and can have a high mortality rate. Although presentation in the perioperative setting in the context of a nonadrenal surgical procedure is infrequent, anaesthetists, intensivists, surgeons, and others who care for such patients must have an awareness of this condition in order to provide timely and appropriate management [3–5]. 2. Case 1 A 68-year-old female, underwent an elective laparoscopic cholecystectomy with an uneventful surgical and anaesthetic course. Her medical history included hypertension for 15 years and a previous surgery for breast carcinoma. Hypertension (BP 205/100?mmHg) was noted in the recovery ward which was partially resolved with opioid analgesia. The following morning she developed atrial fibrillation (rate 170?bpm), hypertension (BP 220/160?mmHg), pulmonary oedema, and lactic acidosis. She became progressively hypotensive and obtunded with a Glasgow coma scale of 4/15 and fixed dilated pupils, requiring intubation, mechanical ventilation, and inotropic vasopressor support with adrenaline and later noradrenaline infusions. Computed tomography scans of brain, chest, and abdomen were reported as unremarkable. Transthoracic echocardiogram revealed severe global left ventricular systolic impairment (ejection fraction <10%). She proceeded to coronary angiography which revealed normal coronary arteries and intra-aortic balloon counterpulsation was instituted.

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