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+A 26-year-old woman was seen in the emergency department (ED) for chest pain and hypertension.
+She was found to have a urinary tract infection and was sent home with an antibiotic and thiazide diuretic.
+Two days later, she returned with epigastric pain, nausea, emesis and myalgias.
+The patient had no significant medical history and denied cardio-respiratory symptoms; however, she complained of a low exercise tolerance for the last year.
+There was no family history of cardiac or pulmonary disease or of sudden cardiac death.
+She was born in the USA and had neither travelled recently nor had any sick contacts.
+On examination, she was hypertensive (170/105 mm Hg), tachycardic (125 bpm), had dry mucous membranes and appeared ill looking.
+She was found to have an elevated serum creatinine of 160 μmol/l (normal 60–110 μmol/l).
+After receiving 1.5 l of intravenous fluids for presumed volume depletion and prerenal azotaemia she became short of breath.
+Crackles were noted on auscultation of her chest and a portable chest film demonstrated hazy infiltrates that likely represented pulmonary oedema.
+She then developed hypotension with systolic pressures in the 90s.
+Non-invasive positive pressure ventilation was initiated.
+An ECG demonstrated sinus tachycardia with a rate of 130 bpm and minimal ST depression on the precordial leads.
+In consultation with a cardiologist, the patient received 40 mg of intravenous furosemide.
+An echocardiogram demonstrated global hypokinesis with a left-ventricular ejection fraction <10% (see figure 1).
+The patient was transferred to the intensive care unit where she became more anxious and tachycardic to 170 bpm.
+She was intubated and sedated.
+Despite the placement of a Foley catheter and administration of intravenous loop diuretics, she remained anuric for the first 12 h of hospitalisation.
+She developed signs of acute kidney injury with a creatinine that increased to 350 μmol/l within the first 24 h of hospitalisation.
+She received norepinephrine and milrinone to improve cardiac output.
+On the second day of hospitalisation, she was evaluated by a cardiologist and cardiothoracic surgeon for emergent circulatory support as she had developed signs of poor tissue perfusion with a lactic acidosis (8.4 mmol/l; normal <2.2 mmol/l) and transaminitis with aspartate aminotransferase/alanine transaminase  >150 IU/l (normal <40 U/l).
+She was taken to the cardiac catheterisation laboratory for emergent right heart catheterisation and biopsy to exclude acute myocarditis.
+Over the next few days, she was gently fluid resuscitated (guided by bioreactance non-invasive cardiac output), the pressors were gradually weaned off and she became non-oliguric.
+She slowly regained renal function and organ perfusion improved with resolution of the lactic acidosis and a decrease in liver transaminases.
+On hospital day 5 she was transferred to the medical ward and was eventually discharged home on non-selective β blockade, an ACE inhibitor and nitrate with planned follow-up at the heart-failure clinic.
+The patient returned to the ED 4 days later with an elevated blood pressure, nausea and abdominal pain.
+A contrast scan of her abdomen revealed pancreatitis and an adrenal mass.
+During her treatment for pancreatitis she began to have paroxysms of headaches, nausea, emesis and abdominal pain with corresponding hypertension to the 220s systolic and tachycardia to 120s with a baseline systolic pressure of 90–110 mm Hg (see figure 2).
+Her urinary and plasma catecholamines were elevated and confirmed on repeat testing.
+She was given aggressive fluid rehydration and α and β blockade for a planned adrenalectomy.
+Prior to surgery her left-ventricular ejection fraction had improved to 55% on medical management (see figure 1).
+Pathology of her adrenal gland was consistent with a non-malignant pheochromocytoma (see figure 3).