2 To our knowledge, only one previous case of severe calcium channel blocker and angiotensin II receptor blocker overdose has been reported in the literature; this reported success with hyperinsulinaemia-euglycaemia, although the data in the paper’s ﬁgures is not convincing [11]. We report a case of severe mixed amlodipine and losartan overdose causing refractory hypotension resistant to all con- ventional vasopressors and hyperinsulinaemia-euglycaemia, but responsive to a metaraminol infusion. 2. Case Report A 50-year-old lady presented to the emergency department (ED) having called the ambulance herself. She reported taking an overdose (handfuls of tablets) of her blood pressure tablets 2 h 45 min previously. The empty packets that she brought with her equated to 104 × 160 mg of losartan (16,640 mg) and 77 × 10 mg of amlodipine (770 mg). She had a past medical history of type 2 diabetes mellitus, hypertension, and morbid obesity (weight 137 kg). At presentation, her airway was patent, with a respiratory rate of 14 breaths/minute and SpO2 of 93% in room air, pulse 100 beats/minute, blood pressure 122/61 mmHg, and temperature 36.4◦C, with Glasgow Coma Score of 15/15. Her ECG was normal. Her initial laboratory results revealed a normal full blood count (FBC), normal renal function including normal potassium, normal liver function tests, and a blood glucose of 10.6 mmol/litre. Shortly after initial assessment in the ED, her blood pressure dropped rapidly to 70/40 mmHg with a pulse of 90 beats/minute that was unresponsive to resuscitation with 2 litres of IV ﬂuid. A central venous line was inserted, and she was transferred to Medical High Dependency. A further 3 litres of intravenous ﬂuid were administered, but she remained anuric and her blood pressure remained at 75 mmHg systolic (mean arterial pressure (MAP) 45– 50 mmHg (see Table 1 and Figures 1 and 2). An arterial line was inserted. Five hours after presentation in the ED, an infusion of noradrenaline (0.1 mcg·kg−1·min−1) the maximum allowed on High Dependency, was started. As this was being setup, metaraminol (boluses of 0.5 mg) were administered produc- ing a transient increase in MAP (Table 1, Figure 2). She also received 20 mLs of 10% calcium gluconate. At this time, pulmonary oedema was seen on X-ray and hypoxia noted (SpO2 91% on FiO2 of 60%). She was started on noninvasive ventilation (NIV) with improvement in oxygenation. Her cognitive function remained normal throughout with a GCS of 15. Advice from the UK National Poisons Information Service at this time was to: give further calcium and start an infusion, try glucagon, continue to uptitrate the ionotropes and consider terlipressin or vasopressin, and to start hyperinsulinaemia-euglycaemia therapy (1 unit/kg bolus then infuse at 0.5 units/kg/hr, increasing to a maximum of 10 units·kg−1·hr−1). Glucagon was given as a bolus of 10 mg followed by an infusion once the patient arrived on ICU. The ﬁrst bolus did Case Reports in Medicine 150 140 130 120 110 )g100 Hm90 (m80 70 60 50 40 30 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90 95100 Time (hrs since ED admission) Pulse bpm Blood pressure mmHg Figure 1: Haemodynamic parameters over the intensive care period. 100 95 4x metaraminol 90 0.5 mg 85 80 )g 7750 H 65 m m 60 ( 55 50 45 40 35 30 Metaraminol boluses until infusion setup 1.4 1.3 1.2 011..91 1−i)n 000000......567483 1−(cggkmm·· 0.2 0.1 0 5 15 25 35 45 55 65 75 85 95 Time (hrs since ED admission) Metaraminol Noradrenaline Adrenaline MAP mmHg Metaraminol bolus Figure 2: Response of MAP in mmHg to infusions over the intensive care period. Note: left y-axis MAP in mmHg, right y- axis infusions of ionotropes in mcg·kg−1·min−1. Arrows show metaraminol boluses. appear to improve the MAP to above 80 mmHg in much the same way as the metaraminol had; however, this was also transient and caused severe vomiting. She was transferred to intensive care 11 hours after presentation to the ED where she was started on vaso- pressin and the noradrenaline was uptitrated initially to 0.05 mcg·kg−1·min−1 and then 0.29 mcg·kg−1·min−1 within the ﬁrst hour with continued increases over the day. Due to a lack of response, adrenaline was also added along with a calcium infusion (Figure 2). Hyperinsulinaemia-euglycaemia was started at 14 hours after admission; after a bolus, the infusion was increased to 6 U·kg−1·hr−1 over the next 12 hrs without any sustained improvement in blood pressure, although there was a slight