Introduction Paracetamol is a common agent taken in deliberate self‐poisoning and in accidental overdose in adults and children. Paracetamol poisoning is the commonest cause of severe acute liver injury. Since the publication of the previous guidelines in 2015, several studies have changed practice. A working group of experts in the area, with representation from all Poisons Information Centres of Australia and New Zealand, were brought together to produce an updated evidence‐based guidance. Main recommendations (unchanged from previous guidelines) The optimal management of most patients with paracetamol overdose is usually straightforward. Patients who present early should be given activated charcoal. Patients at risk of hepatotoxicity should receive intravenous acetylcysteine. The paracetamol nomogram is used to assess the need for treatment in acute immediate release paracetamol ingestions with a known time of ingestion. Cases that require different management include modified release paracetamol overdoses, large or massive overdoses, accidental liquid ingestion in children, and repeated supratherapeutic ingestions. Major changes in management in the guidelines The new guidelines recommend a two‐bag acetylcysteine infusion regimen (200 mg/kg over 4 h, then 100 mg/kg over 16 h). This has similar efficacy but significantly reduced adverse reactions compared with the previous three‐bag regimen. Massive paracetamol overdoses that result in high paracetamol concentrations more than double the nomogram line should be managed with an increased dose of acetylcysteine. All potentially toxic modified release paracetamol ingestions (≥ 10 g or ≥ 200 mg/kg, whichever is less) should receive a full course of acetylcysteine. Patients ingesting ≥ 30 g or ≥ 500 mg/kg should receive increased doses of acetylcysteine.

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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There is a potential role for prehospital pRBC transfusions in an integrated civilian trauma system. The RTS calculated using the initial set of observations may be a useful tool in determining in which patients the administration of prehospital pRBC transfusions would be futile.

The use of droperidol for acute behavioral disturbance in the prehospital setting is associated with fewer adverse events, a shorter time to sedation, and fewer requirements for additional sedation.

Objectives: This study aimed to determine the impact on practice of applying the Extracorporeal Treatments in Poisoning (EXTRIP) Workgroup criteria to lithium toxicity. Method:We retrospectively examined the medical records of patients from three hospitals who presented with chronic or acute on chronic lithium poisoning with a lithium concentration ≥1.3 mmol/L (2008)(2009)(2010)(2011)(2012)(2013)(2014)(2015)(2016)(2017)(2018). We determined which criteria were met by patients and their subsequent course. We developed and validated a method to predict if lithium concentration would be >1mmol/L at 36 hours.Results: There were 111 acute on chronic and 250 chronic lithium toxic patients.Nine patients (2.5%) were treated with haemodialysis. Six chronic patients had neurological sequelae. The "estimated lithium concentration at 36 hours > 1 mmol/L" criterion required pharmacokinetic calculations. A simple nomogram was developed using Estimated Glomerular Filtration Rate (eGFR) and lithium concentration. For chronic toxicity, the nomogram would have correctly predicted lithium concentration >1.4 mmol/L at 36 hours in all except two patients. If EXTRIP criteria were followed, dialysis would have been instituted for 211 patients (58%). However, only 51 patients with chronic toxicity fulfilled both a concentration and a clinical criterion. Late neurological sequelae were observed in five out of six patients who fulfilled a concentration and a clinical criterion on admission, with the sixth meeting these criteria shortly after admission. Conclusions:The EXTRIP criteria are too broad, but minor modifications allow haemodialysis to be targeted to those most at risk of sequelae. Most acute on chronic poisonings do not need haemodialysis, but it might shorten hospital stay in those with very high concentrations. The nomogram accurately predicts the fall in lithium concentration for chronic poisoning. K E Y W O R D S acute on chronic lithium poisoning, chronic lithium toxicity, EXTRIP, haemodialysis, nomogram

Background: Snakebite-associated thrombotic microangiopathy (TMA) occurs in a subset of patients with venom-induced consumption coagulopathy (VICC) following snakebite. Acute kidney injury (AKI) is the commonest end-organ manifestation of TMA. The epidemiology, diagnostic features, outcomes, and effectiveness of interventions including therapeutic plasma-exchange (TPE), in snakebite-associated TMA are poorly understood. Methods: We reviewed all patients with suspected or confirmed snakebite recruited to the Australian Snakebite Project (2004-2018 inclusive), a prospective cohort study, from 202 participating Australian hospitals across the country. TMA was defined as anemia with schistocytosis. Results: 2069 patients with suspected snakebite were enrolled, with 1158 (56.0%) systemically envenomed, of which 842 (72.7%) developed VICC, from which 104 (12.4%) developed TMA. Of those systemically envenomed, TMA occurred in 26% (13/50) taipan, 17% (60/351) brown, and 8% (16/197) tiger snakebites. Thrombocytopenia was present in 90% (94/104) of TMA cases, and a further eight (8%) had a > 25% decrease in platelets from the presentation. Patients with TMA were significantly older than non-TMA patients with versus 41 [24-55] years, median [IQR], p < 0.0001). AKI developed in 94% (98/104) of TMA patients, with 34% (33/98) requiring dialysis (D-AKI). There were four deaths. In D-AKI TMA cases, eventual dialysis-free survival (DFS) was 97% (32/33). TPE was used in five D-AKI cases, with no significant difference in DFS or time to independence from dialysis. >90-day follow-up for 25 D-AKI cases (130 person-years) showed no end-stage kidney disease but 52% (13/25) had ! stage 3 chronic kidney disease (CKD). Conclusion:Our findings support a definition of snakebite-associated TMA as anemia with schistocytosis and either thrombocytopenia or >25% drop in platelet count. AKI occurring with snakebite-associated TMA varied in severity, with most achieving DFS, but with a risk of long-term CKD in half. We found no evidence of benefit for TPE in D-AKI.