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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]

The article focuses on toxicology and presents advice for emergency clinicians. Topics include the importance of seeking support from readily accessible resources and treating illicit drugs with supportive care; and the use of activated charcoal, the administration of naloxone in opioid overdose cases along with guidance on the use of sodium bicarbonate in the treatment of toxic ingestions.

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]

The international boundaries to medical education are becoming less marked as new technologies such as multiuser videoconferencing are developed and become more accessible to help bridge the communication gaps. The Global Educational Toxicology Uniting Project (GETUP) is aimed at connecting clinicians in countries with established clinical toxicology services to clinicians in countries without clinical toxicologists around the globe. Centers that manage or consult on toxicology cases were registered through the American College of Medical Toxicology website via Survey Monkey ®. Data was analyzed retrospectively from February 2014 to January 2015. Google hangouts ® was used as the main conferencing software, but some sites preferred the use of Skype ®. Registration data included contact details and toxicology background and qualifications. Thirty sites in 19 different countries in Australasia, Europe, Africa, and America were registered. Twenty-eight (93 %) sites were located in a major urban center, one (3.5 %) site in a major rural center and one (3.5 %) a private practice. Expectations of GETUP included sharing toxicology cases and education (30, 100 % of sites), assistance with toxicology management guidelines (2, 7 %), assistance with providing a toxicology teaching curriculum in languages other than English (2, 7 %), and managing toxicology presentations in resource-poor settings, international collaboration, and toxicovigilance (2 sites, 7 %). Twenty-two conferences were performed during the first 12 months with a mean of 3 cases per conference. GETUP has connected countries and clinical units with and without toxicology services and will provide a platform to improve international collaboration in clinical toxicology. [ABSTRACT FROM AUTHOR]

Context. Oral oxycodone/naloxone preparations are designed to reduce the incidence of constipation associated with oxycodone use. The low oral bioavailability (< 2%) of naloxone makes the precipitation of the acute opioid withdrawal symptoms unlikely following oral oxycodone/naloxone exposure. The incidence of acute opioid withdrawal symptoms following both oral and intravenous administration of oxycodone/naloxone preparations has not been described.Objective.The aim of the study was to investigate the incidence and circumstances associated with oxycodone/naloxone-induced acute opioid withdrawal.Methods.An observational case series of acute opioid withdrawal following oxycodone/naloxone administration were selected from all calls received by the Victoria Poisons Information Centre from January 2012 to December 2014. Data collected included patient demographics, reported symptoms, type of caller, intentional or accidental exposure and advice given.Results.There were 107 reported exposures to oxycodone/naloxone preparations. Route of exposure was oral in 92 (86%) and intravenous injection of crushed tablets in 14 (14%) of cases, respectively. Nine callers had a history of long-standing opioid treatment and developed withdrawal symptoms with oral oxycodone/naloxone. Temporal relationship between first dose, increased dose and chewing tablets was described. There were 14 exposures to crushed oxycodone/naloxone tablets injected intravenously; all precipitated an acute withdrawal state.Discussion.The development of opioid withdrawal symptoms with intravenous injection of oxycodone/naloxone is likely a result of bypassing first-pass metabolism. Withdrawal symptoms after ingesting increased dose, first dose or chewing oxycodone/naloxone suggests that there is a systemic absorption of naloxone in opioid-dependent callers.Conclusion.Oxycodone with naloxone tablets can lead to acute opioid withdrawal symptoms if crushed and injected parentally. First dose, increased dose and chewing of these opioid–naloxone combination tablets in opioid-dependent people can also result in acute opioid withdrawal symptoms or diminished pain relief. [ABSTRACT FROM PUBLISHER]

Six opiate-dependent drug users presented to the local emergency department within a 10-day period with symptoms of severe opioid withdrawal immediately following intravenous use of recently acquired street 'heroin'. The withdrawal picture was similar to that described in patients undergoing rapid opioid detoxification, suggesting that the substance injected was contaminated with an opiate antagonist. A number of potential compounds are discussed, including naltrexone and buprenorphine, and recommendations for the medical management of severe opiate withdrawal within an emergency setting are outlined. [Lubman DI, Koutsogiannis Z, Kronborg I. Emergency management of inadvertent accelerated opiate withdrawal in dependent opiate users. Drug Alcohol Rev 2003;2:433 - 436] [ABSTRACT FROM AUTHOR]

The article presents a case study of a 60-year-old who was presented to the emergency department (ED) due to a short illness and severe vomiting. He underwent electrocardiograph (ECG) that showed polymorphic ventricular tachycardia or torsades de pointes (TdP). The patient had a maintenance of methadone as long-term opioid substitution therapy (OST). The patient had no chest pain.

The article presents case study of a 31-year-old man presented to the emergency department (ED) to cease his frequent gamma-hydroxybutyric acid (GHB) usage. It mentions that attempts at weaning sedation were unsuccessful because of reappearance of physiological signs of a severe withdrawal state. It also highlights early recognition of potential for progressive neuropsychiatric manifestations and physiological dysfunction.

A 28-year-old primigravida was referred to a maternale fetal specialist because a fetal ultrasound at 20 weeks showed oligohydramnios, absence of the right kidney and a small echogenic left kidney with poor corticomedullary differentiation, and intrauterine growth restriction. She had a history of lethargy throughout her pregnancy and a normocytic anaemia with a haemoglobin level of 95 g/L (reference interval [RI], 97–148 g/L) at 24 weeks' gestation and 88 g/L (RI, 95–150 g/L) at 30 weeks' gestation. Her white cell count and platelet count were normal at 24 weeks' and 30 weeks' gestation. Liver and renal function test results, and serum vitamin B12, folate and ferritin levels were also within normal limits at both 24 weeks' and 30 weeks' gestation. Chorionic venous sampling performed at 24 weeks did not detect any significant genomic abnormalities. At 30 weeks' gestation, the maternal blood film showed basophilic stippling and her blood lead level (BLL) was high at 3.2 µmol/L (RI, < 0.48 µmol/L) or 67 µg/dL (RI, < 10 µg/dL). The toxicology unit was consulted and chelation was commenced, including oral dimercaptosuccinic acid (DMSA) at a dose of 10 mg/kg three times a day for 5 days followed by 10 mg/kg twice daily for 14 days. Three weeks after chelation, her BLL was 0.7 µmol/L (14.4 µg/dL). For the previous 6 months, the patient had been taking two tablets per day of an Ayurvedic medicine, prescribed by a practitioner in India, that she was self-importing to Australia. Analysis of these tablets (performed by DTS Food Laboratories, a National Association of Testing Authorities-accredited laboratory) using inductively coupled plasma mass spectrometry, a process used to detect metals and non-metals, showed a lead content of 47%, small amounts of mercury (1.7%), and arsenic (< 0.01%). Urine arsenic and mercury levels were within normal limits. No other sources of lead exposure or ingestion were found. Fetal growth improved after chelation therapy commenced; however, further ultrasound scans of the fetus showed diminished left renal tissue with progression to anhydramnios by 30 weeks' gestation. By 34 weeks' + 5 days' gestation, there was no fetal renal tissue visible on ultrasound. The family received extensive counselling from the neonatal and renal specialists and the paediatric toxicologist, with consideration as to whether to dialyse the baby if chelation was needed and if the expected related respiratory failure was considered survivable postnatally. Three days before an elective caesarean section at 39 weeks, the mother received intravenous calcium disodium edetate 40 mg/kg twice daily to decrease her lead concentrations before delivery. She gave birth to a 3.14 kg baby who had severe hypoxic and hypercapnic respiratory failure and a small right pneumothorax as a result of pulmonary hypoplasia, and severe contractures with bilateral dislocated hips, each resultant of the antenatal anhydramnios. The baby did not have typical facies of Potter sequences or other congenital abnormalities associated with Potter syndrome. Renal ultrasound showed no left renal tissue and a severely dysplastic right kidney of 1 cm diameter. The cord BLL at delivery was low at 0.37 mmol/L (8.0 µg/dL). Given the low BLL, chelation was not initiated. The baby died 2 days later from severe respiratory failure owing to poor antenatal pulmonary development, a result of the severe renal dysgenesis. At autopsy, the BLL was 0.55 mmol/L (11.5 µg/dL) and there was severely hypoplastic and multicystic renal tissue bilaterally (right kidney, 15 g; left kidney, 16 g), with normal ureters and bladder. Three weeks' postpartum, the mother's BLLwas 0.8 mmol/L (17.3 µg/dL). [ABSTRACT FROM AUTHOR]

A letter to the editor is presented which discusses a case of pulmonary haemorrhage associated with the use of rivaroxaban.