Objective: There is little recent published data characterising methamphetamine intoxication. The present study aims to describe the clinical effects, management, complications and disposition of patients with methamphetamine exposure. Methods: This is a retrospective review of patients presenting with methamphetamine intoxication to an ED in 2016. All presentations were extracted from a relational database and each medical record reviewed. Demographics, clinical features, complications and disposition were extracted. Results: There were 378 presentations of 329 patients (234 men [71%]), median age 31 years (range 16-68 years). The most common clinical effect was acute behavioural disturbance, occurring in 295 (78%) presentations. This was successfully managed with oral sedation alone in 180 (61%) patients, with the remainder receiving parenteral sedation. Other effects included tachycardia in 212 (56%), hypertension in 160 (42%) and hyperthermia in 17 (5%) presentations. No antihypertensives were given. One patient was actively cooled. Complications included 21 (30%) presentations with rhabdomyolysis and 41 (13%) presentations with acute kidney injury. There were two seizures, three intracranial bleeds and one myocardial infarction. The majority (317 [84%]) of patients were managed solely within the ED. The median length of stay was 14 h. There were 41 (11%) mental health admissions. Two deaths occurred: one following an out-ofhospital cardiac arrest and the other a subarachnoid haemorrhage. Conclusion: The main toxicity seen with methamphetamines is acute behavioural disturbance, which is managed well with sedation. Complications, apart from rhabdomyolysis and acute kidney injury, are rare. Most patients are managed within the ED and discharged home.

With rising use worldwide, pregabalin is increasingly implicated in poisoning deaths. We aimed to investigate the clinical effects and complications of pregabalin poisoning. Methods: This is a retrospective review of patients presenting with pregabalin poisoning to two tertiary toxicology units from 1 July 2014 to 30 June 2019. Patients were identified from prospective databases maintained by both units and data were extracted from these in addition to medical records. Results: There were 488 presentations in 413 patients (237 [57%] male) over the five-year period. The median age was 41 years (IQR 31-50 years). Deliberate selfpoisonings accounted for 342 (70%) presentations, with 121 (25%) recreational exposures. Recreational exposures increased over the period from 2 (4%) in the first year to 54 (39%) presentations in the final year. The median dose of pregabalin was 1200 mg (IQR 600-3000 mg, range 75-16 800 mg). Co-ingestions occurred in 427 (88%) presentations, with sedating agents being co-ingested in 387 (79%)-most commonly opioids and benzodiazepines in 201 (41%) and 174 (36%) presentations respectively. Coma (GCS < 9) occurred in 89 (18%) cases, with 52 (11%) patients being intubated. Only one (0.2%) of these patients had not co-ingested a sedating agent. Hypotension occurred in 26 (5%) cases, all with co-ingestants. Seizures occurred in 11 (2%) cases, 3/59 (5%) in pregabalin-only overdoses. The median length of stay was 16.5 hours (IQR 10-25 hours). Conclusions: Pregabalin overdose does not cause severe toxicity, but rather mild sedation and, uncommonly, seizures. Coma is common in the presence of sedating co-ingestants. Recreational use is increasing. K E Y W O R D S drug abuse, overdose and poisoning, toxicology 1 | INTRODUCTION Pregabalin is a gamma-aminobutyric acid analogue that binds to voltage-gated calcium channels to inhibit the release of excitatory neurotransmitters, which accounts for its antinociceptive, anticonvulsant and anxiolytic properties. 1,2 Over the last decade, pregabalin has been increasingly prescribed for neuropathic pain, as well as a number of off-label indications including anxiety, mood instability and withdrawal syndromes. 1-4 With the broadening of both approved and off-label indications, pregabalin use has increased worldwide over the last The authors confirm that the PI for this paper is Katherine Isoardi and that she had direct clinical responsibility for patients.

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Aim The effects of methamphetamine intoxication on the kidney are not well reported. We aimed to investigate acute kidney injury (AKI) associated with methamphetamine intoxication, in particular its severity, duration and association with rhabdomyolysis. Methods This is a prospective observational series of methamphetamine‐intoxicated patients presenting to an Emergency Department. Patients self‐reporting recent methamphetamine use, with a positive urine drug screen and an elevated creatinine, were eligible for the study. Urinary neutrophil gelatinase‐associated lipocalin (NGAL) was measured, and serum creatinine, creatine kinase and cystatin C concentrations were performed on arrival and at several time points until discharge from hospital. Demographic and clinical data were obtained from the medical records. Results There were 634 presentations with methamphetamine intoxication over a 10‐month period, with 73/595(12%) cases having an elevated serum creatinine concentration on arrival. Fifty presentations in 48 patients were included in the study. Most patients (85%) were male with a median age of 32 years. The median serum creatinine concentration on presentation was 125 μmol/L (IQR:113‐135 μmol/L) with 45 (90%) presentations meeting diagnostic criteria for AKI. Concurrent rhabdomyolysis occurred in 22 (44%) presentations with a median CK of 2695 U/L (IQR:1598‐5060 U/L). Cystatin C was elevated (> 0.98 mg/L) in 18 cases. An elevated NGAL concentration (>150 μg/L) was present in five (10%) cases. No patients required dialysis. The median length of stay was 19 hours (IQR 14‐24 hours). Conclusion AKI is common in methamphetamine intoxication. The kidney injury is relatively mild and short‐lived, resolving with crystalloid therapy.

Background: Previous studies of paracetamol overdose treatment show that a 2-bag, 20-h intravenous (IV) acetylcysteine regimen decreased the incidence of non-allergic anaphylactic reactions compared to the 3bag, 21 h IV regimen, but have not examined efficacy of the 20-h 2 bag regimen. Methods: This was a multi-centre observational study of paracetamol overdose presentations treated with a 2-bag IV acetylcysteine regimen (200 mg/kg over 4 h, 100 mg/kg over 16 h) compared to a 3-bag regimen, performed from 2009 to 2019. Patients were referred from the emergency department to the inpatient toxicology units for continued management. For the primary non-inferiority analysis: subjects had single, acute ingestions, a serum paracetamol-concentration performed 4 to 8-h post-ingestion. The primary outcome was development of acute liver injury (ALI), defined as peak ALT>150 U/L; and > double admission baseline ALT (for presentations within 24 h post-overdose). Secondary outcomes included adverse reactions to acetylcysteine (cutaneous and systemic). Finding: Out of 6419 paracetamol overdoses, 2763 received acetylcysteine. For the primary analysis, 1003 received the 2-bag and 783 the 3-bag acetylcysteine regimen. When presentation bloods were performed 4 to 8-h post-overdose, 21 (3.1%) developed ALI with the 2-bag regimen vs 16 (2.9%) with the 3-bag regimen (Difference: 0.2%, 95%CI:-1.6 to 2.2). The incidence of hepatotoxicity was: 1.2% (n = 8) with the two-bag regimen and 1.6% (n = 9) with the three-bag regimen (Difference -0.4%, 95%CI -1.75, 0.91). When presentation bloods were performed 8 to 24-h post-overdose, 70 (21%) developed ALI with the 2-bag regimen vs 46 (23%) with the 3-bag regimen (Difference: -2%, 95%CI -9.12 to 5.36). There were significantly less cutaneous and systemic non-allergic anaphylactic reactions recorded after treatment with the two-bag than the three-bag regimen (1.3% [n = 17] and 7.1% [n = 65], Difference: -5.8%, 95%CI -7.6 to -4.0, p < 0.0001), respectively. Interpretation: A two-bag intravenous acetylcysteine regimen was found to be non-inferior to the three-bag regimen with regards to efficacy in preventing acute liver injury for early presentations of paracetamol

The reduction in average LOS is similar to results previously published by two Australian toxicology units over 15 years ago. Despite changes in healthcare delivery since this time, these results continue to support the efficiency and associated cost saving of a dedicated toxicology unit in managing poisoned patients.

Severe toxicity following an acute ingestion of a large amount of methotrexate is rarely reported. The development of toxicity was unexpected in this case given methotrexate's pharmacokinetics and the patient's normal renal function. The serum methotrexate concentrations were below the treatment threshold of the folinic acid rescue therapy nomogram suggesting that the nomogram should not be relied on in acute ingestions. Large acute oral methotrexate poisoning can result in systemic toxicity and folinic acid therapy should be provided in ingestions >1000 mg.

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