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Barium poisoning is rare but potentially severe. We describe a case of acute barium carbonate poisoning with cardiac arrest, managed with intravenous potassium, dialysis and endoscopic removal of retained ceramic glazes. A 38-year-old woman presented with vomiting 90 min after ingesting 3 cups of barium and strontium carbonate. Initial bloods noted potassium 2.8 mmol/L and creatinine 53 μmol/L. Electrocardiogram demonstrated prolonged corrected QT interval 585msec. Initial management included intravenous potassium. Four hours post-ingestion she developed proximal muscle weakness in upper limbs with a potassium of 2.2 mmol/L. At 15 h post-ingestion she developed profound muscle weakness, polymorphic ventricular tachycardia and cardiac arrest. Treatment included defibrillation, endotracheal intubation and continuous veno-venous haemodialysis (CVVHD) for metabolic derangement and enhanced elimination of barium. Chest X-ray 17 h post-ingestion demonstrated a large radio-opaque mass in the stomach, thought to be the ceramic glaze. Endoscopy removed the retained material 41 h post-ingestion. She was extubated 58 h post-ingestion and CVVHD was ceased on day 3. Serum creatinine peaked at 348 μmol/L on day 7, but normalised by discharge. Biphasic barium concentrations were noted, notably 94 μmol/L on admission, 195 μmol/L at 16 h, 95 μmol/L at 20 h, and 193 μmol/L at 30 h post-ingestion. In barium poisoning with hypokalaemia, prompt potassium supplementation is required but rebound hyperkalaemia can occur. Endoscopic removal of ceramic glazes may be useful more than 12 h post-ingestion. Consider extracorporeal methods to enhance barium elimination in severe cases. [ABSTRACT FROM AUTHOR]

Introduction: Beta-adrenoreceptor antagonist (beta-blocker) poisoning is a common overdose which can lead to significant morbidity and mortality. Objective: To evaluate the effects of treatments for beta-adrenoreceptor antagonist poisoning. Methods: Searches were conducted across MEDLINE (1946–26 November 2019, Ovid); Embase (1974–26 November 2019, Ovid); and the Cochrane Central Register of Controlled Trials (CENTRAL, to 26 November 2019) utilising a combination of subject headings and free text. The search strategy identified 15, 553 citations. Two reviewers screened titles and abstracts prior to selecting 141 articles (Kappa on articles included = 0.982, 95% CI 0.980–0.985). Primary outcomes included mortality and improvement in haemodynamic parameters (e.g., heart rate, blood pressure or a composite measure able to quantitate a haemodynamic response). Results: The risk of bias was high for all interventions. Gastric decontamination: Fifteen case reports described the administration of activated charcoal and five detailed the use of gastric lavage. As there was concurrent utilisation of multiple interventions, it was difficult to draw definitive conclusions regarding the relative contribution of these interventions to mortality or survival. Catecholamines, inotropes and vasopressors: The use of catecholamines in treating beta-blocker toxicity was reported in 16 case reports, 3 case series and 2 animal studies. These agents most likely provided a survival benefit and improved haemodynamics. Atropine: Multiple intravenous boluses of atropine were associated with improvement in heart rate and blood pressure in one case report. Calcium: Intravenous calcium was associated with an improvement in haemodynamics in three out of six case reports but in association with multiple other therapies as well as in two animal studies. High-dose insulin euglycaemic therapy: The use of this therapy was associated with mortality benefit in 10 case series. Two case reports showed clear haemodynamic improvement in a timeframe consistent with insulin administration (bolus then continuous infusion). Maintenance dosing ranged from 1 to 10 units/kg/h of insulin. However, it is unclear whether high-dose insulin euglycaemic therapy improved haemodynamic response above catecholamines and other inotropic agents in humans. Hypoglycaemia and hypokalemia were commonly observed adverse effects. Glucagon: Glucagon was associated with minor improvements in haemodynamics through an increase in heart rate in two cases series, nine case reports and five animal studies. Methylthioninium chloride (methylene blue): Four case reports reported an association with improvement in haemodynamics following administration of methylene blue but in the setting of co-ingestion with amlodipine. Intravenous lipid emulsion therapy: There was variable response to intravenous lipid emulsion therapy reported in 10 case series, 5 animal studies and 21 case reports. Lignocaine: There were four case reports showing variable response to lignocaine in arrhythmias secondary to beta-blocker toxicity. Other treatments: Fructose diphosphate, levosimendan and amrinone did not provide a mortality or significant haemodynamic benefit in three animal studies and nine case reports.. Veno-arterial extracorporeal membrane oxygenation: Veno-arterial extracorporeal membrane oxygenation was associated with improved survival in patients with severe cardiogenic shock or cardiac arrest in an observational study and four cases series. Dialysis: The evidence of four case reports suggest haemodialysis may assist in the management of massive overdose of specific water-soluble beta-blockers (e.g., atenolol) by improving elimination; however, a survival or haemodynamic benefit was not established. Pacing: One case series and a single case report showed the utility of temporary overdrive cardiac pacing to prevent arrhythmias in sotalol toxicity. Conclusions: Catecholamines, vasopressors, high-dose insulin euglycaemic therapy and veno-arterial extracorporeal membrane oxygenation were associated with reduced mortality. However, it must be acknowledged that multiple treatments were often given simultaneously. Haemodynamic improvements in blood pressure and cardiac output were seen with the use of catecholamines, vasopressin and high-dose insulin euglycaemic therapy. Evidence for treatment recommendations is almost entirely drawn from very low- to low-quality studies and subject to bias. However, it is reasonable to have a graduated response to cardiovascular instability beginning with intravenous fluids, commencement of a single or a combination of catecholamine inotropes and vasopressors depending upon the type of haemodynamic compromise (bradycardia, left ventricular dysfunction, vasodilation). High-dose insulin euglycaemic therapy can be introduced as an adjunctive inotrope and lastly, more invasive methods such as veno-arterial extracorporeal membrane oxygenation should be considered in cases unresponsive to other therapies. [ABSTRACT FROM AUTHOR]

The use of beta-adrenoceptor antagonists for treatment of tachydysrhythmias secondary to sympathomimetic agents is controversial due to concerns of "unopposed alpha receptor stimulation." Labetalol is a dual alpha 1 and beta1/beta 2 adrenoceptor antagonist. We report the case of a 33-year-old male who developed rapid atrial fibrillation with a ventricular rate of 151 beats per minute in the setting of methamphetamine use. He received intravenous labetalol 10 mg on five occasions over a 6.5 h period, which slowed his ventricular rate and eventually resulted in restoration of sinus rhythm. Administration of labetolol did not produce a clinically significant rise in blood pressure. Combination alpha and beta blockade using labetalol may be an effective and safe treatment option in patients with methamphetamine associated supraventricular tachydysrhythmias. [ABSTRACT FROM AUTHOR]