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To assess the accuracy and marginal value of quantitative D-dimer testing for diagnosing venom-induced consumption coagulopathy (VICC) in people bitten by Australian snakes.Analysis of data for suspected and confirmed cases of snakebite collected prospectively by the Australian Snakebite Project, 2005-2019, from 200 hospitals across Australia.1363 patients for whom D-dimer was quantitatively assessed within 24 hours of suspected or confirmed snakebite.Diagnostic performance of quantitative D-dimer testing for detecting systemic envenoming with VICC (area under the receiver operating characteristic curve, AUC); optimal D-dimer cut-off value (maximum sum of sensitivity and specificity).D-dimer values exceeded 2.5 mg/L within three hours of the bite for 95% of patients who developed VICC, and were lower than 2.5 mg/L for 95% of non-envenomed patients up to six hours after snakebite. The AUC for diagnosing envenoming with VICC on the basis of quantitative D-dimer testing within six hours of snakebite was 0.97 (95% CI, 0.96-0.98; 944 patients). Diagnostic performance increased during the first three hours after snakebite; for quantitative D-dimer testing at 2-6 hours, the AUC was 0.99 (95% CI, 0.99-1.0); with a cut-off of 2.5 mg/L, sensitivity was 97.1% (95% CI, 95.0-98.3%) and specificity 99.0% (95% CI, 97.6-99.6%) for VICC. For 36 patients with normal international normalised ratio (INR) and activated partial thromboplastin time (aPTT) values 2-6 hours after snakebite, the AUC was 0.97 (95% CI, 0.93-1.0); with a cut-off of 1.4 mg/L, sensitivity was 94% (95% CI, 82-99%) and specificity 96% (95% CI, 94-97%). In all but one of 84 patients who developed VICC-related acute kidney injury, D-dimer values exceeded 4 mg/L within 24 hours of the bite.D-dimer concentrations assessed 2-6 hours after snakebite, with a cut-off value of 2.5 mg/L, could be useful for diagnosing envenoming with VICC.

Objectives To assess the numbers of paracetamol overdose-related hospital admissions and deaths in Australia since 2007-08, and the overdose size of intentional paracetamol overdoses since 2004. Design, setting Retrospective analysis of data on paracetamol-related exposures, hospital admissions, and deaths from the Australian Institute of Health and Welfare National Hospital Morbidity Database (NHMD; 2007-08 to 2016-17), the New South Wales Poisons Information Centre (NSWPIC; 2004-2017), and the National Coronial Information System (NCIS; 2007-08 to 2016-17). Participants People who took overdoses of paracetamol in single ingredient preparations. Main outcome measures Annual numbers of reported paracetamol-related poisonings, hospital admissions, and deaths; number of tablets taken in overdoses. Results The NHMD included 95 668 admissions with paracetamol poisoning diagnoses (2007-08 to 2016-17); the annual number of cases increased by 44.3% during the study period (3.8% per year; 95% CI, 3.2-4.6%). Toxic liver disease was documented for 1816 of these patients; the annual number increased by 108% during the study period (7.7% per year; 95% CI, 6.0-9.5%). The NSWPIC database included 22 997 reports of intentional overdose with paracetamol (2004-2017); the annual number increased by 77.0% during the study period (3.3% per year; 95% CI, 2.5-4.2%). The median number of tablets taken increased from 15 (IQR, 10-24) in 2004 to 20 (IQR, 10-35) in 2017. Modified release paracetamol ingestion report numbers increased 38% between 2004 and 2017 (95% CI, 30-47%). 126 in-hospital deaths were recorded in the NHMD, and 205 deaths (in-hospital and out of hospital) in the NCIS, with no temporal trends. Conclusions The frequency of paracetamol overdose-related hospital admissions has increased in Australia since 2004, and the rise is associated with greater numbers of liver injury diagnoses. Overdose size and the proportion of overdoses involving modified release paracetamol have each also increased.

Objective: To describe the epidemiology, treatment and adverse events after snakebite in Australia. Design: Prospective, multicentre study of data on patients with snakebites recruited to the Australian Snakebite Project (2005-2015) and data from the National Coronial Information System. Setting, participants: Patients presenting to Australian hospitals with suspected or confirmed snakebites from July 2005 to June 2015 and consenting to participation. Main outcome measures: Demographic data, circumstances of bites, clinical effects of envenoming, results of laboratory investigations and snake venom detection kit (SVDK) testing, antivenom treatment and adverse reactions, time to discharge, deaths. Results: 1548 patients with suspected snakebites were enrolled, including 835 envenomed patients (median, 87 per year), for 718 of which the snake type was definitively established, most frequently brown snakes (41%), tiger snakes (17%) and red-bellied black snakes (16%). Clinical effects included venom-induced consumption coagulopathy (73%), myotoxicity (17%), and acute kidney injury (12%); severe complications included cardiac arrest (25 cases; 2.9%) and major haemorrhage (13 cases; 1.6%). There were 23 deaths (median, two per year), attributed to brown (17), tiger (four) and unknown (two) snakes; ten followed out-of-hospital cardiac arrests and six followed intracranial haemorrhages. Of 597 SVDK test results for envenomed patients with confirmed snake type, 29 (4.9%) were incorrect; 133 of 364 SVDK test results for non-envenomed patients (36%) were false positives. 755 patients received antivenom, including 49 non-envenomed patients; 178 (24%), including ten non-envenomed patients, had systemic hypersensitivity reactions, of which 45 (6%) were severe (hypotension, hypoxaemia). Median total antivenom dose declined from four vials to one, but median time to first antivenom was unchanged (4.3 hours; IQR, 2.7-6.3 hours). Conclusions: Snake envenoming is uncommon in Australia, but is often severe. SVDKs were unreliable for determining snake type. The median antivenom dose has declined without harming patients. Improved early diagnostic strategies are needed to reduce the frequently long delays before antivenom administration.

OBJECTIVES: To report the frequency and clinical outcomes of Amanita phalloides poisoning in the Australian Capital Territory and New South Wales, and the treatments used (including silibinin). DESIGN, SETTING AND PATIENTS: Retrospective case series of patients admitted to public hospitals in Canberra and Sydney for suspected A. phalloides poisoning between 1999 and 2012 (identified from hospital records and calls to the New South Wales Poisons Information Centre). Main outcome measures: Frequency of poisoning and the clinical outcomes. RESULTS: Twelve patients presented with a history suggesting A. phalloides poisoning, 10 with probable poisoning and two with possible poisoning. Eight of those with probable poisoning developed significant hepatotoxicity and four died. Silibinin was administered to nine of those with probable poisoning (the other presented before 2005). Maintaining silibinin supply became a challenge during two clusters of poisoning. Eight of the patients with probable poisoning were not long-term residents of the ACT, and six were immigrants from Asia. CONCLUSIONS: The mortality rate due to A. phalloides poisoning in this case series was high despite treatment according to current standards, including use of silibinin, and the frequency of hepatotoxicity was more than double that for the previous decade. Ongoing public health campaigns are required. Language: en

Snakebite is a potential medical emergency and must receive high-priority assessment and treatment, even in patients who initially appear well. Patients should be treated in hospitals with onsite laboratory facilities, appropriate antivenom stocks and a clinician capable of treating complications such as anaphylaxis. All patients with suspected snakebite should be admitted to a suitable clinical unit, such as an emergency short-stay unit, for at least 12 hours after the bite. Serial blood testing (activated partial thromboplastin time, international normalised ratio and creatine kinase level) and neurological examinations should be done for all patients. Most snakebites will not result in significant envenoming and do not require antivenom. Antivenom should be administered as soon as there is evidence of envenoming. Evidence of systemic envenoming includes venom-induced consumption coagulopathy, sudden collapse, myotoxicity, neurotoxicity, thrombotic microangiopathy and renal impairment. Venomous snake groups each cause a characteristic clinical syndrome, which can be used in combination with local geographical distribution information to determine the probable snake involved and appropriate antivenom to use. The Snake Venom Detection Kit may assist in regions where the range of possible snakes is too broad to allow the use of monovalent antivenoms. When the snake identification remains unclear, two monovalent antivenoms (eg, brown snake and tiger snake antivenom) that cover possible snakes, or a polyvalent antivenom, can be used. One vial of the relevant antivenom is sufficient to bind all circulating venom. However, recovery may be delayed as many clinical and laboratory effects of venom are not immediately reversible. For expert advice on envenoming, contact the National Poisons Information Centre on 13 11 26.

Objective: To describe the clinical features and laboratory findings in patients with definite red-bellied black snake (RBBS; Pseudechis porphyriacus) bites, including correlation with results of venom assays. Design, patients and setting: Prospective cohort study of patients with definite RBBS bites, recruited to the Australian Snakebite Project from January 2002 to June 2010. Main outcome measures: Clinical and laboratory features of envenoming; peak venom concentrations and antivenom treatment. Results: There were 81 definite RBBS bites; systemic envenoming occurred in 57 patients (70%) and local envenoming alone occurred in one patient. Systemic envenoming was characterised by local envenoming in 55 patients (96%), systemic symptoms in 54 patients (95%), anticoagulant coagulopathy with a raised activated partial thromboplastin time (aPTT) in 35 patients (61%) and myotoxicity in seven patients (12%). One patient required non-invasive ventilation for severe myotoxicity that resulted in muscle weakness. Three patients developed local ulceration. There were no deaths. Twenty-two envenomed patients (39%) received tiger snake or black snake antivenom, and administration within 6 hours of the bite was associated with normalisation of the aPTT. Eight patients (36%) had immediate hypersensitivity reactions to antivenom, including one case of anaphylaxis. The median peak venom concentration in 37 systemically envenomed patients with serum available was 19 ng/mL (interquartile range, 12–50 ng/mL; range, 3–360 ng/mL), which did not correlate with clinical severity. In 17 patients who received antivenom and had venom concentration measured, no venom was detected in serum after the first antivenom dose, including nine who were given one vial of tiger snake antivenom. Conclusion: RBBS envenoming caused local effects, systemic symptoms, anticoagulant coagulopathy and, uncommonly, myotoxicity. One vial of tiger snake or black snake antivenom appears to be sufficient to remove venom and neutralise reversible effects, but

To determine which laboratory tests are first associated with severe envenoming after a snakebite, when (ie, how long after the bite) the test results become abnormal, and whether this can determine a safe observation period after suspected snakebite.Prospective cohort study of 478 patients with suspected or confirmed snakebite recruited to the Australian Snakebite Project from January 2002 to April 2009, who had at least three sets of laboratory test results and at least 12 hours of observation in hospital after the bite. Severe envenoming was defined as venom-induced consumption coagulopathy (VICC), myotoxicity, neurotoxicity or thrombotic microangiopathy.International normalised ratio (INR), activated partial thromboplastin time (aPTT), creatine kinase (CK) level, and neurological examination.There were 240 patients with severe envenoming, 75 with minor envenoming and 163 non-envenomed patients. Of 206 patients with VICC, 178 had an INR1.2 (abnormal) on admission, and the remaining 28 had an INR1.2 within 12 hours of the bite. Of 33 patients with myotoxicity, a combination of CK250 U/L and an abnormal aPTT identified all but two cases by 12 hours; one of these two was identified within 12 hours by leukocytosis. Nine cases of isolated neurotoxicity had a median time of onset after the bite of 4 hours (range, 35 min - 12 h). The combination of serial INR, aPTT and CK tests and repeated neurological examination identified 213 of 222 severe envenoming cases (96%) by 6 hours and 238 of 240 (99%) by 12 hours.Laboratory parameters (INR, aPTT and CK) and neurological reassessments identified nearly all severe envenoming cases within 12 hours of the bite, even in this conservative analysis that assumed normal test results if the test was not done.

A woman with acute poisoning from extended-release paracetamol presented at 14.5 hours post-ingestion. The paracetamol's absorption phase and elimination half-life appeared prolonged, with peak blood concentration occurring at 20 hours post-ingestion, requiring an extended course of intravenous N-acetylcysteine. Current treatment recommendations, based on experience with a different formulation in the United States, may not be appropriate for the Australian formulation.

Paracetamol is involved in a large proportion of accidental paediatric exposures and deliberate self-poisoning cases, although subsequent hepatic failure and death are both uncommon outcomes. The optimal management of most patients with paracetamol overdose is usually straightforward. However, several differing nomograms and varying recommendations regarding potential risk factors for hepatic injury introduce complexity. In order to reconcile management advice with current Australasian clinical toxicology practice, revised guidelines have been developed by a panel of clinical toxicologists consulting to the poisons information centres in Australia and New Zealand using a workshop and consultative process. This article summarises the rationale for the recommendations made in these new guidelines.

Objective To study drug prescribing by brand name versus generic name in an Australian teaching hospital. Results Overall, 53% of drugs were prescribed by brand name. Brand names were preferred when they were shorter and easier to remember and spell, when there was only one brand on the market, and when the brand name ended in an x. Conclusion Doctors might be encouraged to prescribe generically if generic names were devised using the same principles marketers use for devising brand names.

OBJECTIVE: To examine the morbidity and mortality associated with self-poisoning with different drug classes. DESIGN: Prospective cohort study with limited follow-up. Retrospective analysis of coronial data. SETTING: Primary and tertiary referral toxicology centre covering Newcastle and Lake Macquarie, Australia, 1987-1992. RESULTS: There were 1969 admissions after ingestion of 3724 substances (2424 prescription drugs and 1300 non-prescription items). The coroner investigated 83 drug-related deaths. Only 12 of these people presented to hospital and, for most of these, death was inevitable at presentation. The most frequently ingested substances were benzodiazepines, alcohol, paracetamol, antidepressants, neuroleptics and anticonvulsants. Since 1980, the percentage of self-poisonings involving benzodiazepines has fallen, while it has risen for those involving antidepressants. Over 50% of deaths were due to tricyclic antidepressants or opioid analgesics. CONCLUSIONS: As death usually occurs out of hospital, interventions to decrease mortality from self-poisoning must focus on prevention, and targeting drugs that are frequently taken or frequently lethal in overdose. Consideration should be given to the use of antidepressants that are safer in overdose. The use of antidepressants, barbiturates or chloral hydrate as sedatives should be discouraged. Language: en