Current Awareness in Clinical Toxicology Editors: Damian Ballam Msc and Allister Vale MD

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Current Awareness in Clinical Toxicology Editors: Damian Ballam MSc and Allister Vale MD

May 2016

CONTENTS General Toxicology 8 Metals 33 Management 16 Pesticides 35 Drugs 19 Chemical Warfare 37 Chemical Incidents & 28 Plants 37 Pollution Chemicals 29 Animals 38

CURRENT AWARENESS PAPERS OF THE MONTH

Efficacy and effectiveness of anti-digoxin antibodies in chronic digoxin poisonings from the DORA study (ATOM-1) Chan BS, Isbister GK, O'Leary M, Chiew A, Buckley NA. Clin Toxicol 2016; online early: doi: 10.1080/15563650.2016.1175620: Context We hypothesized that in chronic digoxin toxicity, anti-digoxin antibodies (Fab) would be efficacious in binding digoxin, but this may not translate into improved clinical outcomes. Objective This study aims to investigate changes in free digoxin concentrations and clinical effects on heart rate and potassium concentrations in chronic digoxin poisoning when anti-digoxin Fab are given. Materials and methods This is a prospective observational study. Patients were recruited if they have been treated with anti-digoxin Fab for chronic digoxin poisoning. Data was entered into a standardised prospective form, supplemented with medical records. Their serum or plasma was collected, analysed for free and bound digoxin and free anti-digoxin Fab concentrations. Results From September 2013 to February 2015, 36 patients (median age, 78 years; 22 females)

Current Awareness in Clinical Toxicology is produced monthly for the American Academy of Clinical Toxicology by the Birmingham Unit of the UK National Poisons Information Service, with contributions from the Cardiff, Edinburgh, and Newcastle

Units.

The NPIS is commissioned by Public Health England

were recruited from 18 hospitals. Median heart rate (HR) was 49 beats/min. Initial median digoxin and potassium concentrations were 4.7 nmol/L (3.6 µg/L) (range: 2.3–11.2 nmol/L) and 5.3 mmol/L (range: 2.9–9.2 mmol/L) respectively. Beta-blockers (n = 18), calcium antagonists (n = 6), spironolactone and/or angiotensin blocking agents (n = 24) were also used concomitantly. Renal impairment and gastrointestinal symptoms were present in 31 (86%) and 22 (63%) patients respectively. Five patients died from conditions unrelated to digoxin toxicity. Median change in HR was 8 beats/min post-Fab with no effect on blood pressure; they were 4, 10 and 17 beats/min for the 1, 2 and 3 vials of anti-digoxin Fab groups respectively. Concomitant treatments with potassium lowering agents (12/36) and inotropic drugs (7/36) were used. Gastrointestinal effects resolved in all 22 patients. The median decrease for potassium was 0.3 mmol/L. Digoxin concentration reduced from 3.8 to 0 nmol/L post-Fab. There was a rebound observed in the free digoxin concentration in 25 patients but none had associated clinical deterioration. Conclusions One to two vials of anti-digoxin Fab initially bound all free digoxin confirming Fab efficacy. However, this was associated with only a moderate improvement in HR and potassium, suggesting bradyarrhythmia and hyperkalaemia may be from other co-morbidities. Full text available from: http://dx.doi.org/10.1080/15563650.2016.1175620

A systematic analysis of methylene blue for drug-induced shock Warrick BJ, Tataru AP, Smolinske S. Clin Toxicol 2016; online early: doi: 10.1080/15563650.2016.1180390: Context Pharmacologically induced shock can be refractory to standard resuscitation. Methylene blue (MB) acts to prevent nitric oxide-mediated vasodilation and may be a potential treatment for refractory shock.Objective: A systematic analysis of the literature to evaluate MB in pharmacologically induced shock. Primary outcome was survival and secondary outcome was hemodynamic improvement. Materials and methods A search of MedLine/PubMed, EMBASE, Cochrane Library, TOXLINE, Google Scholar and Google was performed 10 August 2015 using a combination of text words and keywords related to MB, shock and specific drugs. We included primary literature articles reporting clinical outcomes in humans. Results The searches yielded 928 citations, with 255 exact duplicates. Of the 673 entries screened, 16 citations met study criteria and comprised 17 cases. Calcium channel blockers (CCBs) represented ten cases (six amlodipine, two verapamil, and two diltiazem), atenolol three cases as coingestant with amlodipine, five metformin, one ibuprofen, and one multidrug (quetiapine, carbamazepine, valproic acid, oxazepam, and fluoxetine). Twelve patients survived and nine had hemodynamic improvement following MB administration. Four did not respond to MB but survived with other advanced resuscitative measures. None of the seven cases had BP improvement and four died when lipid was given prior to MB, compared to one death and nine cases of BP improvement when lipid was not given. In all cases, MB was used after failing several other treatments. Bolus doses ranging from 1 to 3 mg/kg, with repeat boluses or maintenance infusions. Reported adverse events were temporary self- limited blue discolorations. Conclusion While there are compelling cases describing an improved hemodynamic status following MB,

there are also several cases without observed change. Currently, there is not enough evidence available to recommend the routine administration of MB in refractory pharmacologically induced shock. Full text available from: http://dx.doi.org/10.1080/15563650.2016.1180390

Epidemiology and clinical features of toxicity following recreational use of synthetic cannabinoid receptor agonists: a report from the United Kingdom National Poisons Information Service Waugh J, Najafi J, Hawkins L, Hill SL, Eddleston M, Vale JA, Thompson JP, Thomas SHL. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1171329: Context Toxicity from the use of synthetic cannabinoid receptor agonists (SCRAs) has been encountered increasingly frequent in many countries. Objective To characterise presentation rates, demographic profiles and reported clinical features for users of SCRAs referred by health professionals in the United Kingdom to the National Poisons Information Service (NPIS), to compare reported toxicity between commonly used branded products, and to examine the impact of legal control measures on enquiry numbers. Methods NPIS telephone enquiry records were searched for SCRA-related terms for the 8-year period 1st January 2007 to 31st December 2014, consolidating multiple enquiries about the same case into a single record. Demographic data, reported exposure details, clinical features and poisoning severity were analysed, excluding cases where SCRA exposure was unlikely. Results Enquiries to the NPIS were made concerning 510 individuals relating to probable SCRA use, with annual numbers increasing year on year. Most patients were male (80.8%) and <25 years old (65.1%). Common clinical features reported in the 433 (84.9%) patients reporting SCRA use without other substances included tachycardia (n = 73, 16.9%), reduced level of consciousness (n = 70, 16.2%), agitation or aggression (n = 45, 10.4%), vomiting (n = 30, 6.9%), dizziness (n = 26, 6.0%), confusion (n= 21, 4.8%), mydriasis (n = 20, 4.6%) and hallucinations (n = 20, 4.6%). The Maximum Poisoning Severity Score (PSS) indicated severe toxicity in 36 cases (8.3%). Legal control of "second generation" SCRAs did not affect the rate of growth in enquiry numbers or the proportion with severe toxicity. The three most commonly reported products were "Black Mamba" (n= 88, 20.3%), "Pandora's Box" (n= 65, 15.0%) and "Clockwork Orange" (n= 27, 6.2%). Neurological and general features were recorded more often with "Clockwork Orange" than for "Black Mamba" and "Pandora's Box", but moderate or severe toxicity was significantly less common after reported use of this product. Conclusions Enquiries about SCRA-related toxicity have become increasingly frequent in the UK in spite of legal controls and commonly involve younger males. Differences in the patterns of toxicity associated with different branded preparations may occur, although further work with larger patient numbers is needed to confirm this. Full text available from: http://dx.doi.org/10.3109/15563650.2016.1171329

Four analytically confirmed cases of use of third-generation synthetic cannabinoid receptor agonists incorporating an adamantyl group Rook W, Ford L, Vale A. Clin Toxicol 2016; online early: doi: 10.1080/15563650.2016.1175005: Full text available from: http://dx.doi.org/10.1080/15563650.2016.1175005

Difference of the clinical course and outcome between dapsone-induced methemoglobinemia and other toxic-agent- induced methemoglobinemia Kim Y-J, Sohn CH, Ryoo SM, Ahn S, Seo DW, Lee Y-S, Lee JH, Oh BJ, Lim KS, Kim WY. Clin Toxicol 2016; online early: doi: 10.1080/15563650.2016.1178759: Context Acquired methemoglobinemia is a potentially fatal condition that leads to tissue hypoxia. Although the clinical features of methemoglobinemia depend on the methemoglobin levels, the clinical course would differ depending on the causative agents. Objective We attempted to clarify this issue by comparing the clinical course of methemoglobinemia caused by dapsone and that caused by other toxic agents. Materials and methods A retrospective case–control study was performed. All patients with methemoglobinemia and who were admitted to the emergency department (ED) of our hospital from 1 January 2002 to 31 December 2014 were included. Results Of the 34 patients with methemoglobinemia, 15 ingested dapsone (14 with acute overdose and one with chronic therapeutic use) and 19 had been exposed to other toxic agents, such as sodium nitrites, indoxacarb, primaquine, and lidocaine. The clinical characteristics and the course of dapsone-induced and other toxic-agent-induced methemoglobinemia were compared. There was no significant difference in clinical presentation and methemoglobin level (38.5% vs. 35.0%, p = 0.456) upon their ED arrival between the two groups. However, the methemoglobin level after use of methylene blue and the total dose of methylene blue were higher in patients with dapsone-induced methemoglobinemia than in those with other agent-induced methemoglobinemia (11.9% vs. 1.7%, p = 0.001, 455 mg vs. 144 mg, p = 0.006). The majority of dapsone-induced methemoglobinemia (93.3%) required more than 72 h for normalization of the methemoglobin level, despite the use of methylene blue. Five of the study patients died due to multiorgan failure, and all of whom were inpatients with dapsone-induced methemoglobinemia. Conclusion The clinical course of dapsone-induced methemoglobinemia was worse than that of other toxic-agent-induced methemoglobinemia despite no significant difference in their initial clinical presentation. Continuous treatment with serial monitoring of the serum methemoglobin is necessary for patients with dapsone-induced methemoglobinemia. Full text available from: http://dx.doi.org/10.1080/15563650.2016.1178759

A prospective study of ketamine versus haloperidol for severe prehospital agitation Cole JB, Moore JC, Nystrom PC, Orozco BS, Stellpflug SJ, Kornas RL, Fryza BJ, Steinberg LW, O'Brien-Lambert A, Bache-Wiig P, Engebretsen KM, Ho JD. Clin Toxicol 2016; online early: doi: 10.1080/15563650.2016.1177652: Context Ketamine is an emerging drug for the treatment of acute undifferentiated agitation in the prehospital environment, however no prospective comparative studies have evaluated its effectiveness or safety in this clinical setting. Objective We hypothesized 5 mg/kg of intramuscular ketamine would be superior to 10 mg of intramuscular haloperidol for severe prehospital agitation, with time to adequate sedation as the primary outcome measure. Methods This was a prospective open label study of all patients in an urban EMS system requiring chemical sedation for severe acute undifferentiated agitation that were subsequently transported to the EMS system's primary Emergency Department. All paramedics were trained in the Altered Mental Status Scale and prospectively recorded agitation scores on all patients. Two 6-month periods where either ketamine or haloperidol was the first-line therapy for severe agitation were prospectively compared primarily for time to adequate sedation. Secondary outcomes included laboratory data and adverse medication events. Results 146 subjects were enrolled; 64 received ketamine, 82 received haloperidol. Median time to adequate sedation for the ketamine group was 5 minutes (range 0.4-23) vs. 17 minutes (range 2–84) in the haloperidol group (difference 12 minutes, 95% CI 9–15). Complications occurred in 49% (27/55) of patients receiving ketamine vs. 5% (4/82) in the haloperidol group. Complications specific to the ketamine group included hypersalivation (21/56, 38%), emergence reaction (5/52, 10%), vomiting (5/57, 9%), and laryngospasm (3/55, 5%). Intubation was also significantly higher in the ketamine group; 39% of patients receiving ketamine were intubated vs. 4% of patients receiving haloperidol. Conclusions Ketamine is superior to haloperidol in terms of time to adequate sedation for severe prehospital acute undifferentiated agitation, but is associated with more complications and a higher intubation rate. Full text available from: http://dx.doi.org/10.1080/15563650.2016.1177652

Plasma paracetamol concentration at hospital presentation has a dose-dependent relationship with liver injury despite prompt treatment with intravenous acetylcysteine Cairney DG, Beckwith HKS, Al-Hourani K, Eddleston M, Bateman DN, Dear JW. Clin Toxicol 2016; 54: 405-10. Context Paracetamol (acetaminophen) overdose is a common reason for emergency hospital admission in the UK and the leading cause of acute liver failure in the Western world.

Currently, the antidote acetylcysteine (NAC) is administered at a dose determined only by body weight without regard for the body burden of paracetamol. Objective To determine whether higher plasma paracetamol concentrations are associated with increased risk of liver injury despite prompt treatment with intravenous NAC. Methods Patients admitted to hospital for treatment with intravenous NAC following a single acute paracetamol overdose entered the study if NAC was commenced within 24 h of drug ingestion (N = 727 hospital presentations). Based on the plasma paracetamol concentration at first presentation to hospital, a series of nomograms were created: 0-100, 101-150, 151- 200, 201-300, 301-500 and over 501 mg/L. The primary endpoints were acute liver injury (ALI – peak serum ALT activity >150 U/L and double the admission value) and hepatotoxicity (peak ALT >1000 U/L). Results ALI and hepatotoxicity were more common in patients with higher admission plasma paracetamol concentrations despite NAC treatment (ALI: nomogram 0–100: 6%, 101–150: 3%, 151–200: 3%, 201–300: 9%, 301–500: 13%, over 501 mg/dL: 27%. p < 0.0001). This dose-response relationship between paracetamol concentration and ALI persisted even in patients treated with NAC within 8 h of overdose (nomogram 0–100: 0%, 101–150: 0.8%, 151–200: 2%, 201–300: 3.6%, 301–500: 12.5%, over 501mg/L: 33%. p < 0.0001) and in patients with normal ALT activity at first presentation (nomogram: 0–100: 0%, 101–150: 1.2%, 151–200: 1.5%, 201–300: 5.3%, 301–500: 10.8% p < 0.0001). Discussion Patients with increased concentrations of plasma paracetamol at hospital presentation are at higher risk of liver injury even when intravenous NAC is promptly administered before there is biochemical evidence of toxicity. Conclusion This study supports theoretical concerns that the current intravenous dose of NAC may be too low in the setting of higher paracetamol exposure. Full text available from: http://dx.doi.org/10.3109/15563650.2016.1159309

Outcomes of patients with premature discontinuation of the 21-h Intravenous N-acetylcysteine protocol after acute acetaminophen overdose Lucyk SN, Yarema MC, Sivilotti MLA, Johnson DW, Nettel-Aguirre A, Victorino C, Bailey B, Dart RC, Heard K, Spyker DA, Rumack BH. J Emerg Med 2016; 50: 629-37. Abstract and full text available from: http://dx.doi.org/10.1016/j.jemermed.2015.12.004

Lipid rescue – Efficacy and safety still unproven Höjer J, Jacobsen D, Neuvonen PJ, Rosenberg PH. Basic Clin Pharmacol Toxicol 2016; online early: doi: 10.1111/bcpt.12607: Abstract and full text available from: http://dx.doi.org/10.1111/bcpt.12607

A review of pitfalls and progress in chelation treatment of metal poisonings Andersen O, Aaseth J. J Trace Elem Med Biol 2016; online early: doi: 10.1016/j.jtemb.2016.03.013: Abstract and full text available from: http://dx.doi.org/10.1016/j.jtemb.2016.03.013

Pediatric exposures to laundry and dishwasher detergents in the United States: 2013–2014 Davis MG, Casavant MJ, Spiller HA, Chounthirath T, Smith GA. Pediatrics 2016; 137: e20154529. Abstract and full text available from: http://dx.doi.org/10.1542/peds.2015-4529

Reactivation of nerve agent-inhibited human acetylcholinesterase by obidoxime, HI-6 and obidoxime+HI-6: kinetic in vitro study with simulated nerve agent toxicokinetics and oxime pharmacokinetics Worek F, Koller M, Thiermann H, Wille T. Toxicology 2016; 350–352: 25-30. Abstract and full text available from: http://dx.doi.org/10.1016/j.tox.2016.05.001

Neurologic, psychiatric, and other medical manifestations of nitrous oxide abuse: a systematic review of the case literature Garakani A, Jaffe RJ, Savla D, Welch AK, Protin CA, Bryson EO, McDowell DM. Am J Addict 2016; online early: doi: 10.1111/ajad.12372: Abstract and full text available from: http://dx.doi.org/10.1111/ajad.12372

Maternal use of selective serotonin-reuptake inhibitors and risk of persistent pulmonary hypertension of the newborn Alwan S, Bandoli G, Chambers CD. Clin Pharmacol Ther 2016; online early: doi: 10.1002/cpt.376: Abstract and full text available from: http://dx.doi.org/10.1002/cpt.376

Ondansetron use in pregnancy and birth defects: a systematic review Carstairs SD. Obstet Gynecol 2016; 127: 878-83. Abstract and full text available from: http://dx.doi.org/10.1097/AOG.0000000000001388

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Pyrethroid insecticides BIOLOGICAL WARFARE AND General RIOT CONTROL AGENTS Cham EYK, Tse JCL, Chong YK, Chen ML, Wong OF, Fung HT. Biological warfare A case of pyrethroid poisoning with clinical presentation Anthrax mimicking organophosphate poisoning. Pshenichnaya N, Mamedova N, Ambalov Y, Usatkin A, Hong Kong J Emerg Med 2016; 23: 47-51. Shmaylenko O, Zhuravlev A. Cutaneous anthrax in the Rostov region of Russia: Magby JP, Richardson JR. difficulties in the clinical diagnostics. Developmental pyrethroid exposure causes long-term Int J Infect Dis 2016; 45 Suppl 1: 472-3. decreases of neuronal sodium channel expression. Neurotoxicology 2016; online early: Chemical warfare doi: 10.1016/j.neuro.2016.04.002: Mustard gas DeSantis-Rodrigues A, Chang Y-C, Hahn RA, Po IP, Zhou P, Deltamethrin Lacey CJ, Pillai A, Young SC, Flowers RA, II, Gallo MA, Laskin JD, Gerecke DR, Svoboda KKH, Heindel ND, Gordon MK. Ben Slima A, Chtourou Y, Barkallah M, Fetoui H, ADAM17 inhibitors attenuate corneal epithelial detachment Boudawara T, Gdoura R. induced by mustard exposure. Endocrine disrupting potential and reproductive Invest Ophthalmol Vis Sci 2016; 57: 1687-98. dysfunction in male mice exposed to deltamethrin.

Hum Exp Toxicol 2016; online early: Panahi Y, Ghanei M, Vahedi E, Mousavi SH, Imani S, doi: 10.1177/0960327116646617: Sahebkar A. Efficacy of probiotic supplementation on quality of life and Lambda cyhalothrin pulmonary symptoms due to sulfur mustard exposure: a randomized double-blind placebo-controlled trial. Deeba F, Raza I, Muhammad N, Rahman H, ur Rehman Z, Drug Chem Toxicol 2016; online early: Azizullah A, Khattak B, Ullah F, Daud MK. doi: 10.3109/01480545.2016.1166250: Chlorpyrifos and lambda cyhalothrin-induced oxidative stress in human erythrocytes: in vitro studies. Toxicol Ind Health 2016; online early: Nerve agents Cadieux CL, Wang H, Zhang Y, Koenig JA, Shih T-M, doi: 10.1177/0748233716635003: McDonough J, Koh J, Cerasoli D.

Probing the activity of a non-oxime reactivator for Prallethrin acetylcholinesterase inhibited by organophosphorus nerve Bashini MM, Rajavel VP, Rahulan V. agents. Complications and management of attempted suicide by Chem Biol Interact 2016; online early: intrapleural injection of prallethrin. doi: 10.1016/j.cbi.2016.04.002: Indian J Crit Care Med 2016; 20: 182-4. Coban A, Carr RL, Chambers HW, Willeford KO, Chambers JE.

Comparison of inhibition kinetics of several Botnariu G, Birsan C, Podoleanu C, Moldovan C, Stolnicu S, organophosphates, including some nerve agent Chiriac A. surrogates, using human erythrocyte and rat and mouse Skin necrosis caused by prallethrin-A worldwide used brain acetylcholinesterase. insecticide. Toxicol Lett 2016; 248: 39-45. Environ Toxicol Pharmacol 2016; 43: 103-4. Worek F, Koller M, Thiermann H, Wille T. Rodenticides Reactivation of nerve agent-inhibited human acetylcholinesterase by obidoxime, HI-6 and obidoxime+HI-6: Marashi SM. kinetic in vitro study with simulated nerve agent What is the real cause of hepatic dysfunction after zinc toxicokinetics and oxime pharmacokinetics. phosphide containing rodenticide poisoning? Toxicology 2016; 350352: 25-30. Indian J Gastroenterol 2016; online early: doi: 10.1007/s12664-016-0640-5: VX Salerno A, Bolzinger M-A, Rolland P, Chevalier Y, Josse D, Zinc phosphide Briançon S. Gunaratne WMSN, Wijeratne AT, Pilapitiya SD, Pickering emulsions for skin decontamination. Siribaddana SH. Toxicol In Vitro 2016; 34: 45-54. A case of severe zinc phosphide poisoning. Ceylon Med J 2016; 61: 42-4. PLANTS Gelsemium elegans (Heartbreak grass) Marashi SM. Xiang H, Zhou YJ, Huang PL, Yu CN, Liu J, Liu LY, He P. What is the real cause of hepatic dysfunction after zinc Lethal poisoning with Gelsemium elegans in Guizhou, phosphide containing rodenticide poisoning? China. Indian J Gastroenterol 2016; online early: Public Health 2016; online early: doi: 10.1007/s12664-016-0640-5: doi: 10.1016/j.puhe.2016.02.031:

Mushrooms and other fungi Chippaux J-P, Akaffou MH, Allali BK, Dosso M, Bakkum M, van Cruijsen H, Kooter AJ. Massougbodji A, Barraviera B. A 39-year-old woman with a mushroom intoxication. The 6th international conference on envenomation by Neth J Med 2016; 74: 136. snakebites and scorpion stings in Africa: a crucial step for the management of envenomation. Shao D, Tang S, Healy RA, Imerman PM, Schrunk DE, J Venom Anim Toxins Incl Trop Dis 2016; 22: 11. Rumbeiha WK. A novel orellanine containing mushroom Cortinarius Gutiérrez JM, Escalante T, Rucavado A, Herrera C. armillatus. Hemorrhage caused by snake venom metalloproteinases: Toxicon 2016; 114: 65-74. a journey of discovery and understanding. Toxins (Basel) 2016; 8: 93.

Mycotoxins Hamza M, Idris MA, Maiyaki MB, Lamorde M, Chippaux J- Taevernier L, Veryser L, Roche N, Peremans K, Burvenich P, Warrell DA, Kuznik A, Habib AG. C, Delesalle C, De Spiegeleer B. Cost-effectiveness of antivenoms for snakebite Human skin permeation of emerging mycotoxins envenoming in 16 countries in West Africa. (beauvericin and enniatins). PLoS Negl Trop Dis 2016; 10: e0004568. J Expos Sci Environ Epidemiol 2016; 26: 277-87. Suthari S, Raju VS. Rhododendron japonicum (Japanese Antidote botanicals for snake bites from Koyas of Warangal Azalea) District, Telangana, India. J Herbs Spices Med Plants 2016; 22: 57-68. Koda R, Honma M, Suzuki K, Kasai A, Takeda T, Narita I, Yoshida K. Hypotension and bradycardia caused by the inadvertent Tan KY, Tan CH, Fung SY, Tan NH. ingestion of Rhododendron japonicum. Neutralization of the principal toxins from the venoms of Intern Med 2016; 55: 839-42. Thai Naja kaouthia and Malaysian Hydrophis schistosus: insights into toxin-specific neutralization by two different

antivenoms. Ricinus communis (Castor oil plant) Toxins (Basel) 2016; 8: 86. de Hann P, Reidinga-Saenen LM, Korporaal-Heijman JA. Intoxication by ingestion of castor beans. Wood D, Sartorius B, Hift R. Neth J Crit Care 2016; 24: 20-2. Ultrasound findings in 42 patients with cytotoxic tissue damage following bites by South African snakes. ANIMALS Emerg Med J 2016; online early: doi: 10.1136/emermed- 2015-205279: Fish/marine poisoning Ciguatera Atractaspididae (Burrowing asps) Farrell H, Zammit A, Manning J, Shadbolt C, Szabo L, Tilbury CR, Verster J. Harwood DT, McNabb P, Turahui JA, van den Berg DJ. A fatal bite from the burrowing asp Atractaspis corpulenta Clinical diagnosis and chemical confirmation of ciguatera (Hallowell 1854). fish poisoning in New South Wales, Australia. Toxicon 2016; 118: 21-6. Commun Dis Intell Q Rep 2016; 40: E1-E6. Crotalinae (Pit vipers) Jellyfish Mong R, Tan HH. Friedel N, Scolnik D, Adir D, Glatstein M. Snakebite by the shore pit viper (Trimeresurus Severe anaphylactic reaction to mediterranean jellyfish purpureomaculatus) treated with polyvalent antivenom. (Ropilhema nomadica) envenomation: case report. Wilderness Environ Med 2016; online early: doi: Toxicol Rep 2016; 3: 427-9. 10.1016/j.wem.2016.01.001:

Scorpions Elapidae Chippaux J-P, Akaffou MH, Allali BK, Dosso M, Lim AY, Singh PN, Isbister GK. Massougbodji A, Barraviera B. Severe rhabdomyolysis from red-bellied black snake The 6th international conference on envenomation by (Pseudechis porphyriacus) envenoming despite antivenom. snakebites and scorpion stings in Africa: a crucial step for Toxicon 2016; 117: 46-8. the management of envenomation. J Venom Anim Toxins Incl Trop Dis 2016; 22: 11. Padula AM, Winkel KD. Red-bellied black snake (Pseudechis porphyriacus) Furtado SS, Belmino JFB, Diniz AGQ, Leite RS. envenomation in the dog: diagnosis and treatment of nine Epidemiology of scorpion envenomation in the state of cases. Ceará, Northeastern Brazil. Toxicon 2016; 117: 69-75. Rev Inst Med Trop Sao Paulo 2016; 58: 1-5. Viperinae (True vipers) Snake bites Su M, Hines EQ. Ajay Kumar S, Vinay Kumar MS, Raghavendra Babu YP, Letter in response to "hyperglycemia is a risk factor for Mahadeshwara Prasad DR. high-grade envenomations after European viper bites An unusual site for a snakebite. (Vipera spp.) in children". Med Leg J 2016; online early: Clin Toxicol 2016; online early: doi: 10.1177/0025817216645043: doi: 10.3109/15563650.2016.1166230:

INDEX 2,4-dinitrophenol ...... 24 Chemical incidents ...... 29 Acetaminophen ...... 27 Chemical warfare, general ...... 37 Acetylcysteine ...... 17 Chemicals, general ...... 29 Acrolein ...... 35 Chlorine ...... 30 Acrylamide ...... 29 Chlorpyrifos ...... 36 Air pollution ...... 28 Ciguatera ...... 38 Alcohol ...... 29 Clonidine ...... 19 Alpha-diketones ...... 29 Cocaine...... 23 Aluminium ...... 33 Codeine ...... 27 Aluminium phosphide ...... 35 Colchicine ...... 23 Amfetamines ...... 20 Copper sulphate ...... 30 Aminophylline ...... 18 Corrosives ...... 30 Amiodarone ...... 20 Corticosteroids ...... 23 Amisulpride ...... 21 Crotalinae ...... 38 Amitriptyline ...... 28 Cyanide ...... 30 Amlodipine ...... 22 Cyanohydrins ...... 31 Anabolic steroids ...... 20 Dapsone ...... 23 Anaesthetics ...... 20 Deltamethrin ...... 37 Analgesics ...... 20 Dermal toxicity ...... 9 Analytical toxicology ...... 8 Designer drugs ...... 23 Animals, general ...... 38 Detergents ...... 31 Anisodamine ...... 18 Developmental toxicology ...... 9 Anthrax ...... 37 Dexamethasone ...... 23 Antiarrhythmic drugs ...... 20 Dexamfetamine ...... 19 Antibiotics ...... 21 Dextromethorphan ...... 24 Anticholinergic drugs ...... 21 Diacetylmorphine...... 24 Anticoagulants ...... 21 Diazepam ...... 22 Anticonvulsants ...... 21 Dichlorvos ...... 36 Antidepressants ...... 21 Diclofenac ...... 26 Antidotes ...... 17 Dietary supplements ...... 24 Antifungal drugs ...... 21 Digoxin ...... 24 Antihistamines ...... 21 Diquat ...... 36 Antimalarial drugs ...... 21 Domperidone ...... 24 Antineoplastic drugs ...... 21 Doxapram ...... 19 Antipsychotics ...... 21 Driving under the influence ...... 10 Antivenom ...... 17 Dronabinol ...... 19 Antiviral drugs ...... 22 Drugs, general ...... 19 Arsenic ...... 34 E-cigarettes ...... 31 Asbestos...... 29 Ecstasy ...... 20 Atractaspididae ...... 38 Elapidae ...... 38 Atrazine ...... 36 Epidemiology...... 10 Baclofen ...... 22 Ethanol ...... 29 Belimumab ...... 25 Ethnic remedies ...... 24 Benzene ...... 29 Ethylene glycol ...... 31 Benzodiazepines ...... 22 Exhaust fumes ...... 28 Benzoic acid ...... 29 Extracorporeal treatments ...... 19 Benzylpiperazine ...... 22 Fab fragments ...... 17 Beta-blockers ...... 22 Fenethylline ...... 24 Betahistine ...... 22 Fipronil ...... 35 Biological warfare...... 37 Fish/marine poisoning ...... 38 Biomarkers ...... 8 Flame retardants ...... 31 Bisphenol A ...... 30 Flecainide...... 21 Bleomycin ...... 21 Flumazenil ...... 17 Body packers ...... 8 Fluoride ...... 31 Buprenorphine ...... 18 Forensic toxicology ...... 11 Bupropion ...... 21 Formaldehyde ...... 31 Burrowing asps ...... 38 Fungicides ...... 35 Cadmium ...... 34 Gamma hydroxybutyrate ...... 24 Caffeine...... 22 Gasoline ...... 32 Calciferol ...... 28 Gelsemium elegans ...... 37 Calcium channel blockers...... 22 Genotoxicity ...... 11 Cannabis ...... 22 Glycols ...... 31 Carbamate insecticides ...... 35 Haemodialysis ...... 19 Carbon monoxide ...... 30 Hallucinogenic drugs ...... 24 Carcinogenicity ...... 8 Haloperidol ...... 19 Cardiotoxicity ...... 8 Heartbreak grass ...... 37 Carvedilol ...... 22 Hepatotoxicity ...... 11 Castor oil plant ...... 38 Herbal medicines ...... 24 Ceramics ...... 30 Herbicides ...... 36 Chelating agents ...... 17 Heroin ...... 24

Hyperbaric oxygen therapy ...... 17 Paraformaldehyde ...... 35 Hypoglycaemics ...... 25 Paraquat ...... 36 Ibuprofen ...... 26 Perfluorinated compounds ...... 32 Immunosuppressants ...... 25 Persulphates ...... 32 Inhalation toxicity ...... 12 Pesticides and cancer...... 35 Insulin ...... 19 Pesticides, general ...... 35 Iodine ...... 31 Petrol...... 32 Japanese Azalea ...... 38 Phenelzine ...... 25 Jellyfish ...... 38 Phenol ...... 32 Kaolin ...... 31 Phthalate esters ...... 32 Ketamine ...... 25 Picaridin ...... 36 Kinetics ...... 12 Pit vipers ...... 38 Kratom ...... 25 Plants, general ...... 37 Lambda cyhalothrin ...... 37 Poison information centres ...... 15 Lamotrigine ...... 21 Poisons information ...... 15 Lead...... 34 Polybrominated diphenyl ethers ...... 32 Levamisole ...... 25 Polychlorinated biphenyls ...... 32 Levetiracetam ...... 25 Polycyclic aromatic hydrocarbons ...... 32 Levobupivacaine ...... 20 Prallethrin ...... 37 Lipid emulsion therapy ...... 18 Promethazine ...... 22 Lithium ...... 34 Propanil ...... 36 Loratadine ...... 21 Propofol ...... 19 Management, general ...... 16 Psychiatric aspects ...... 15 Manganese ...... 34 Pyrethroid insecticides, general ...... 37 Marijuana ...... 22 Radiation ...... 32 MDMA ...... 20 Reprotoxicity ...... 15 Medication errors ...... 12 Rhododendron japonicum ...... 38 Mefloquine ...... 21 Ricinus communis ...... 38 Mephedrone ...... 25 Risk assessment ...... 15 Mercury ...... 34 Rodenticides ...... 37 Metabolism ...... 12 Salbutamol ...... 27 Metals, general ...... 33 Salicylates ...... 27 Metformin ...... 25 Scorpions ...... 38 Methanol ...... 31 Smoke ...... 32 Methotrexate ...... 21 Snake bites ...... 38 Methoxetamine ...... 25 Sodium arsenate ...... 32 Methoxyflurane ...... 25 Sodium nitroprusside ...... 27 Methyl iodide ...... 31 Solvents ...... 32 Methylene blue ...... 18 SSRIs and SNRIs ...... 27 Methylene chloride ...... 31 Substance abuse ...... 27 Methylisothiazolinone ...... 31 Sugammadex ...... 19 Methylthioninium chloride ...... 18 Suicide ...... 16 Monoamine oxidase inhibitors ...... 25 Synthetic cannabinoids ...... 23 Monoclonal antibodies ...... 25 Tacrolimus ...... 25 Muscle relaxants ...... 25 Thiocolchicoside ...... 20 Mushrooms ...... 38 Ticagrelor ...... 28 Mustard gas ...... 37 Tilmicosin...... 21 Mycotoxins ...... 38 Tobacco ...... 32 Nalmefene ...... 19 Tocilizumab ...... 25 Naloxone ...... 18 Toluene ...... 33 Nanoparticles ...... 32 Toxicology, general ...... 8 Nephrotoxicity ...... 12 Trichloroethylene ...... 33 Nerve agents ...... 37 Triclosan ...... 33 Neurotoxicity ...... 12 Tricyclic antidepressants ...... 28 Nicotine ...... 25 True vipers...... 38 Nitrous oxide ...... 26 Turpentine ...... 33 NSAIDs ...... 26 Uranium ...... 35 Occupational toxicology ...... 13 Venlafaxine ...... 27 Ocular toxicity ...... 14 Verapamil ...... 22 Omeprazole ...... 26 Viperinae ...... 38 Ondansetron ...... 26 Vitamins...... 28 Opioids ...... 26 Volatile organic compounds ...... 33 Organochlorine pesticides, general ...... 36 VX ...... 37 Organophosphorus insecticides, general ...... 36 Warfarin ...... 21 Oximes ...... 18 Water ...... 33 Oxybutynin ...... 21 Yellow phosphorus ...... 33 Oxygen ...... 32 Zinc phosphide ...... 37 Paediatric toxicology ...... 14 alpha-tocopherol ...... 17 Paracetamol ...... 27

The NPIS is commissioned by Public Health England