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帕可(氨磺必利片)意中毒造成严重的心脏毒性包括QT间期延长及尖端扭转
Amisulpride deliberate self-poisoning causing severe cardiac toxicity including QT prolongation and torsades de pointes
Geoffrey K Isbister, Lindsay Murray, Sally John, L Peter Hackett, Tedo Haider, Phebe OMullane, Sophie Gosselin and Frank Daly
Med J Aust 2006; 184 (7): 354-356.
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Although clinical trials of the antipsychotic amisulpride revealed no cardiac adverse effects, four patients with severe cardiac toxicity after overdose were reported to Australian poisons information centres in 2004–2005. All four had QT prolongation over 500 ms, two had rate-dependent bundle branch block, two developed torsades de pointes, and one died after cardiac arrest. Pending further studies, we recommend electrocardiogram assessment until at least 16 h after amisulpride overdose and, if QT interval is prolonged, cardiac monitoring until the patient is clinically well and conduction intervals are normal.
Clinical records
Patient 1
A 39-year-old woman presented to a rural hospital 2 hours after ingesting 24 g of amisulpride (therapeutic dose, 50–1200 mg/day), and unknown quantities of nitrazepam and diazepam. On examination, she was drowsy with a Glasgow Coma Score (GCS) of 14, heart rate of 100 beats per min (bpm), and systolic blood pressure of 70 mmHg. Activated charcoal (50 g) and intravenous normal saline (2 L) were administered, and the hypotension resolved. She was transferred to a tertiary emergency department.
On arrival, 7 h after the overdose, her condition remained unchanged. An electrocardiogram (ECG) showed sinus rhythm, heart rate of 67 bpm, QRS interval of 128 ms, prolonged QT interval of 560 ms and bifid T waves (Box 1). Twelve hours after ingestion, her level of consciousness decreased (GCS, 4), and broad complex tachycardia was observed on the electrocardiography monitor and subsequent ECG. No hypotension was recorded. She was intubated, hyperventilated, given NaHCO3, magnesium and calcium gluconate, and transferred to the in
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