A 61-year-old man presented to the emergency department following an intentional overdose of 32 g of amisulpride (therapeutic dose: 50-1,200 mg/day). On arrival, he was unconscious (Glasgow Coma Score 3), had poor respiratory effort, hypotension (blood pressure 90/40 mm Hg) and hypothermia (temperature 32.4°C). An ECG demonstrated sinus rhythm, a heart rate of 90 bpm, with intermittent selfresolving ventricular tachycardia and a prolonged QTc interval (corrected QT time, calculated with Bazett' s formula, of 431 msec). Laboratory results included: Na + 141 mmol/L, Cl -102 mmol/L, K + 3.9 mmol/L and an ionised Ca 2+ of 1.17 mmol/L. Blood gases showed a lactic acidosis with a pH of 7.05, base deficit of -15 mmol/L and a lactate of 12 mmol/L. The initial plasma amisulpride level was found to be 50 mg/L. Immediate treatment consisted of intubation, mechanical ventilation and fluid resuscitation. The patient required vasopressor therapy with noradrenaline at a rate of 0.25 µg/kg/min. Despite receiving 5 litres of Hartmann' s solution and maintaining a central venous pressure of around 12 cm H 2 O, his noradrenaline requirements increased to 0.56 µg/kg/min.He was transferred to the intensive care unit (ICU) where haemodynamic assessment using the LiDCO Rapid © technique demonstrated a low cardiac output. Considered together with lactic acidosis, this suggested low global tissue perfusion. This was treated with dobutamine, while continuous veno-venous haemofiltration (CVVHF) and a simultaneous sodium bicarbonate infusion were initiated to reduce the immediate cardiovascular effects of the low pH. CVVHF was maintained almost continuously, at a dose of 35 mL/kg/h. Accusol 35 (Baxter International Inc.) was used as the buffer solution.The plasma amisulpride level following haemofiltration was higher (59.5 mg/L) than the initial level, suggesting either a haemoconcentration effect or continued absorption.The lactic acidosis resolved over the initial 12 hours, but significant cardiovascular instability was a continuing feature over the next few days. There were four recorded episodes of torsades de pointes, one example of which is shown in Figure 1. One episode required a precordial thump, another direct current shock and others were self-resolving. These episodes resolved following further aggressive therapy, as suggested by TOXBASE, aimed at: • Maintenance of serum potassium, calcium, and magnesium levels at the high end of the normal range • Reduction of the QTc interval by increasing the heart rate above 100 bpm using an isoprenaline infusion. 1 After commencing the isoprenaline infusion, no further episodes of torsades de pointes occurred.The maximum QTc of 725 msec (Figure 2) was recorded at 50 hours post-overdose. It remained elevated at 451 msec in spite of therapy until 190 hours post-overdose.In view of the long-term ventilatory requirements, a tracheostomy was inserted on day eight. The patient was successfully decannulated on day 14 and made an uneventful and complete recovery.A 61-year-old man took an amisulprid...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.