5 Accepted treatments include aggressive fluid resuscitation, the administration of hypertonic sodium bicarbonate and intravenous magnesium. The reported mortality rate from overdoses of class Ic Vaughan Williams anti-arrhythmics is 22.5%. With progressive improvement in these indices and after a period of psychiatric assessment, the patient was discharged home with no obvious sequelae. A degree of ischaemic liver injury was noted, with the serum aspartate transaminase (AST) and alanine transaminase (ALT) peaking at 3,781 and 3,110 IU/l respectively, 60 hours post overdose. The pacing wire was withdrawn, the inotropes weaned and the patient successfully extubated. #Lipid emulsion therapy serial#Twelve hours after the initial presentation, cardiac stability returned serial 12-lead ECGs demonstrated sinus rhythm, a QRS duration of <120 ms and a QT c of <450 ms. Intravenous bicarbonate and ionotropes were continued throughout this period although a temporary transvenous pacing wire was inserted, this was never utilised. Prior to transfer and immediately after the return of cardiac output, a 70 ml bolus of 20% ILE (1.5 ml/kg) was administered, followed by a further 225 ml (0.25ml/kg/min) over the next 20 minutes.įor the next 8 hours, severe cardiovascular instability was observed with the cardiac rhythm frequently alternating between a sinus tachycardia with right bundle branch block, Torsades de Pointes, a Brugada-like syndrome, coarse VT and ventricular standstill. Following successful cardiopulmonary resuscitation, she was transferred to a tertiary care centre, intubated, ventilated and with ionotropic support in situ. Despite these interventions, the patient had a VF arrest one hour after presenting to the ED. 8.4% intravenous sodium bicarbonate was also advised in an effort to maintain a pH of 7.45–7.50, along with an infusion of magnesium sulphate (20 mmol). The clinical toxicologist on call recommended intravenous glucagon therapy in view of her bisoprolol ingestion however 4 mg was given intramuscularly. Two 900 ml boluses (20 ml/kg) of 0.9% sodium chloride solution were given and advice sought from the medical toxicology service. The venous pH was 7.55, bicarbonate 24.1 mmol/l and BE +3.0. Her serum sodium was 137 mmol/l, potassium 3.7 mmol/l and magnesium 0.83 mmol/l a four-hour salicylate level was <50 mg/l, while her four-hour paracetamol level was <10 mg/l. The initial 12-lead ECG demonstrated a sinus rhythm (ventricular rate 70 bpm), first-degree AV nodal blockade (PR interval 215 ms), right bundle branch block (QRS duration 164 ms) and a QT c of 452 ms. On arrival, she was alert (GCS 15/15) with a normal respiratory rate (12 breaths per minute) and oxygen saturations of 100% on room air although her heart rate was 65 bpm, she was found to be hypotensive (70/39 mmHg). Her weight was 45 kg and she had no significant medical history. The patient was discharged from the intensive care unit 11 days later with no lasting physiologic sequelae.A 13-year-old girl attended her local emergency department (ED) 90 minutes after consuming 25 mg bisoprolol, 900 mg flecainide and 225 mg aspirin. However, there was a decrease in the frequency of wide-complex tachycardia during the lipid emulsion infusion and a recurrence of wide-complex tachycardia shortly after the infusion was stopped. Twenty percent lipid emulsion was administered intravenously (an initial 150 mL bolus, followed by an infusion at 16 mL/h and a second bolus of 40 mL) over 39 hours (total dose 814 mL) yet resulted in no dramatic changes in hemodynamics or level of consciousness. She had multiple episodes of pulseless wide-complex tachycardia despite conventional treatment with chest compressions, cardioversion, lidocaine, epinephrine, norepinephrine, magnesium sulphate, sodium bicarbonate, activated charcoal, and whole bowel irrigation. Here we report a 25-year-old female presenting with coma and hemodynamic instability following intentional ingestion of amitriptyline. Furthermore, case reports in humans have described the use of lipid therapy to reverse the toxicity of other lipophilic drugs. Intravenous lipid emulsion therapy is an emerging antidote for local anesthetic toxicity, and there is animal evidence that lipid therapy may be efficacious in TCA overdose. Tricyclic antidepressant (TCA) overdose is a leading cause of death among intentional overdoses.
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