Atenolol
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Phaeochromocytoma crisis: case report A 48-year-old woman developed phaeochromocytoma crisis following treatment with atenolol for hypertension and tachycardia. The woman, who complained of 4 years history of epigastric pain was treated with unspecified proton pump inhibitors without any abdominal imaging. Her symptom progressively worsened. Anamnesis revealed completion of treatment for pulmonary tuberculosis 12 years previously. She was a non-smoker. One month prior, she had been admitted for severe headache and forceful heartbeats. Her HR was 120 bpm, and BP was 224/190mm Hg. Physical examination revealed normal neurological and cardiopulmonary systems. She received amlodipine and hydralazine. The symptoms had improved and the systolic BP reduced. Abdominal CT was performed to evaluate the chronic epigastric pain. CT revealed a large heterogeneous enhancing mass with central necrosis in her right upper abdomen. Renal or suprarenal tumours were suspected. Amlodipine and hydralazine were continued. She was referred to urology department for further management. On admission, physical examination and vital signs were measured, which showed HR 120 bpm, BP 170/100mm Hg and regular rhythm. She had mildly pale conjunctiva without any peripheral oedema. Initial blood laboratory test showed mild anaemia and hyponatraemia. Chest radiograph revealed a cardiothoracic ratio of 0.55. Electrocardiogram (ECG) revealed left ventricular hypertrophy, sinus tachycardia and normal axis. Twelve hours following admission, she complained of palpitations. Her HR and BP were 120 bpm and 160/90mm Hg, respectively. She received atenolol 50mg [route not stated] for hypertension and tachycardia. Twelve hours after the single dose of atenolol, she developed sudden dyspnoea and agitation. Her BP increased to 220/120mm Hg, RR was 40 breath/min, HR was 150 bpm and oxygen saturation was 85%. High jugular venous pressure was noted. She had experienced bilateral lung crepitations. Chest radiograph reveled new bilateral patchy infiltrates consistent with acute pulmonary oedema. Urgent ECG showed sinus tachycardia. She was diagnosed with hypertensive crisis and acute pulmonary oedema. The woman required positive pressure ventilation and intubation due to respiratory failure. She also received treatment with nicardipine and furosemide. A transthoracic echocardiography revealed global hypokinesia of the left ventricular wall with left ventricular ejection fraction of 36% consistent with cardiomyopathy. No significant valvular disease was determined. She had increased cardiac markers. Based on the hypertensive crisis following the single dose of atenolol and underlying right upper quadrant mass (phaeochromocytoma), a diagnosis of atenolol induced phaeochromocytoma crisis was made, which resulted in susequent hypertensive crisis, acute pulmonary oedema and cardiomyopathy. She started receiving treatment with prazosin until the BP normalised 12 hours following the onset of hypertensive crisis. Seventy-two hours later, her clinical status showed signif
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