David McCoubrie

Snakebite in Australia: a practical approach to diagnosis and treatment

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.

'Lessons learned': a comparative case study analysis of an emergency department response to two burns disasters

The Royal Perth Hospital (RPH; Perth, Australia) has been the receiving facility for burns patients in two separate disasters. In 2002, RPH received 28 severely injured burns patients after the Bali bombing, and in 2009 RPH received 23 significantly burnt patients as a result of an explosion on board a foreign vessel in the remote Ashmore Reef Islands (840 km west of Darwin). The aim of this paper is to identify the interventions developed following the Bali bombing in 2002 and review their effectiveness of their implementation in the subsequent burns disaster.

Ecstasy-induced acute coronary syndrome: something to rave about.

Ecstasy or 3,4‐methylenedioxymethamphetamine is a commonly used illicit recreational drug, enjoying popularity for its stimulant effects. Although acute coronary syndrome is recognized after cocaine and methamphetamine use, association with Ecstasy use has rarely been reported. We report three cases of significantly delayed acute coronary syndrome and ST elevation myocardial infarction related to ingestion of Ecstasy.

Point‐of‐care testing in snakebite: An envenomed case with false negative coagulation studies

Dear Editor, Early detection of venom-induced consumption coagulopathy (VICC) in Australian snake bite is important for early antivenom administration. However, many patients present to smaller or rural hospitals where on-site laboratory coagulations studies are not available. Point-of-care (POC) devices for an international normalised ratio (INR) and D-dimer have become available and have been used in this setting. A 43-year-old woman presented to a small rural hospital in southwest Western Australia an hour after being bitten while putting her hand in a fish pond. She immediately saw ‘blood on her knuckle’, felt unwell with nausea and vomited twice, experienced chest tightness and felt faint. She did not apply first aid and washed the bite site. She was well on arrival to hospital, with no bleeding, no ptosis and normal vital signs. An INR was performed with a POC device (Alere INRatio2, Alere San Diego, San Diego, CA, USA), which was 1.3 on admission and 1.5 half an hour later. A pressure bandage was applied and she was transferred to a regional base hospital. On arrival at the base hospital 4 h post-bite the patient felt better and the INR was 0.9 on a second POC device (Roche CoaguChek, Roche Diagnostics, Mannheim, Germany). Blood collected at the same time was sent to the on-site laboratory where the INR was unrecordable. On examination there was oozing from the venipuncture site and no neurotoxicity. A snake venom detection kit was positive for tiger snake venom on urine. Two vials of tiger snake antivenom were given and the patient enrolled in the Australian Snakebite Project (ASP) randomised controlled trial of fresh frozen plasma (FFP). The patient was randomised to receive 4 units of FFP given immediately after antivenom. Additional serum and citrate samples were collected for ASP. A D-dimer performed on a POC device (Roche Cobas H232, Roche Diagnostics Limited, Rotkreuz, Switzerland) was 0.38 mg/L (<0.36). The patient had no immediate adverse reaction to antivenom or FFP and had an uneventful recovery, being discharged on day 3. Serial INR results are shown in Figure 1. Serial D-dimers done on the POC device ranged from 0.24 to 0.73 mg/L. The creatine kinase peaked at 432 IU/L. On follow up, the patient had symptoms consistent with mild serum sickness. Tiger snake venom (Notechis spp.) was detected at a concentration of 5.1 ng/mL in serum prior to antivenom and was undetectable post-antivenom. Repeat coagulation studies on admission gave an INR >12, activated partial thromboplastin time (aPTT) >180 s, undetectable fibrinogen and a D-dimer of 812 mg/L (<0.25). At 9 h post-bite, the INR was 2.2, aPTT was 39.5 s, fibrinogen was 0.4 g/L and D-dimer was 458 mg/L. The POC testing results for the INR and D-dimer were incorrect and misleading in this patient with tiger snake envenoming. This might have resulted in delayed treatment if the patient had not been transferred to a hospital equipped for laboratory confirmation of the INR. In addition to identifying problems with POC testing in VICC, the case underlines the importance of the history of a suspected snake bite and early systemic symptoms in the patient. Misleading POC INR results have been reported previously with laboratory-confirmed severe VICC. This suggests that POC testing for INR and D-dimer are likely to be unreliable in VICC and formal laboratory testing is recommended until POC testing devices are formally assessed in VICC. Patients with suspected snakebite should be managed in hospitals with laboratory-based INR and aPTT testing available, or be transferred to a larger hospital. It remains unclear whether this problem applies to all POC testing systems. Currently, no other bedside clotting test is available, including the 20 min whole blood

Correlation of paired plasma and saliva paracetamol levels following deliberate self-poisoning with paracetamol (the Salivary Paracetamol In Toxicology (SPIT) study)

Aim. To determine the correlation between plasma and saliva paracetamol levels following paracetamol deliberate self-poisoning. Methods. Paired plasma and saliva paracetamol levels were measured. Saliva analysis was performed contemporaneously using a colorimetric method. Results. 21 patients (76% female) mean age 28.3 ± 12.9 years (range 15–55) were enrolled. Mean reported paracetamol ingestion was 10.3 g (range 2–20 g). Specimens were collected at a mean of 6.2 ± 3.1 hours post-ingestion (range 4–13 hours) and mean plasma and saliva paracetamol levels were 48 mg/L and 62 mg/L respectively (mean difference 14; 95% CI 5–22; p < 0.004); Pearsons correlation r = 0.95 (p < 0.0001). No patient needing treatment would have been missed using saliva levels only. Conclusion. There is concordance between the indications for treatment of paracetamol deliberate self-poisoning based on plasma and saliva paracetamol levels. Saliva paracetamol levels are typically higher than plasma levels. Further studies involving larger numbers of patients, comparing plasma and saliva paracetamol levels in patients with potentially toxic plasma paracetamol concentrations, would be useful in determining the potential clinical value of this method.

Correlation of paired toxic plasma and saliva paracetamol concentrations following deliberate self‐poisoning with paracetamol

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT • Paracetamol is commonly used in deliberate self poisoning (DSP) and this requires blood sampling to refine risk assessment. If saliva concentrations agreed with plasma concentrations, then this could support the development of non-invasive testing. Our pilot work supports this hypothesis, but was largely confined to nontoxic concentrations. WHAT THIS STUDY ADDS • We found agreement between the indications for treatment of paracetamol DSP based on plasma and saliva paracetamol concentrations. Saliva may hold promise as a non-invasive method to risk stratify paracetamol poisoning. AIMS Paracetamol is commonly used in deliberate self poisoning (DSP) and requires blood sampling to refine risk assessment. We aimed to test the agreement between plasma and saliva paracetamol concentrations in the toxic range in DSP. METHODS Contemporaneous paired plasma and saliva paracetamol concentrations were measured. Saliva was collected using a Sarstedt Salivette® device and the concentration was measured using a colorimetric method. RESULTS Fifty-six patients (44, 78% female) median age 26 years (IQR 20-41) were enrolled. The median reported paracetamol ingestion was 10 g (IQR 6-14). Specimens were collected at a median of 4 h (IQR 4-5.3) post ingestion. The median plasma and saliva paracetamol concentrations were 29 mg l(-1) (IQR 8-110) and 38 mg l(-1) (IQR 10-105) respectively [mean difference 8 mg l(-1) , 95% confidence interval (CI) 2, 14]. Lins concordance correlation was 0.97 (95% CI 0.96, 0.98). There were 15 patients who were treated with N-acetylcysteine. Their median reported paracetamol ingestion was 14 g (IQR 10-23) and samples were collected at a median of 4 h post ingestion. The median plasma and saliva paracetamol concentrations were 167 mg l(-1) (IQR 110-200) and 170 mg l(-1) (IQR 103-210) respectively (mean difference 15 mg l(-1) , 95% CI -4, 35). Lins concordance correlation was 0.94 (95% CI 0.88, 0.99). No patient needing treatment would have been missed using saliva concentrations only. CONCLUSIONS The agreement between the indications for treatment of paracetamol DSP based on plasma and saliva paracetamol concentrations extends into the toxic range, but with slightly lower agreement. Saliva may hold promise as a non-invasive method to risk stratify paracetamol poisoning.

Lesions are seen in young users of stimulant drugs

The editorial by Wallin and Fladby highlights the clinical importance of white matter hyperintensities on magnetic resonance imaging as a marker of small vessel disease in elderly people.1 Prevalence ranges from 11-21% at age 64 …

Teaching neuroimages: ‘Blind drunk’: neuroimaging findings in methanol poisoning

A 34-year-old male presented to the emergency room in a confused state with visual loss following methanol intake. He rapidly progressed to coma requiring intubation. On examination, the patient was unresponsive with fixed dilated pupils, but other brain stem reflexes were present. Arterial blood gases showed pH 6.86, bicarbonate 6 mmol/ l, anion gap elevated at 42 mmol/l and lactate 15 mmol/l. MRI is shown (Fig. 1). The patient had no improvement and died 1 week after admission. The putamen and optic nerves appear to be particularly susceptible to the effect of