Clinical Toxicology ISSN: 1556-3650 (Print) 1556-9519 (Online) Journal homepage: https://www.tandfonline.com/loi/ictx20 39th International Congress of the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT) 21-24 May 2019, Naples, Italy To cite this article: (2019): 39th International Congress of the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT) 21-24 May 2019, Naples, Italy, Clinical Toxicology, DOI: 10.1080/15563650.2019.1598646 To link to this article: https://doi.org/10.1080/15563650.2019.1598646 Published online: 16 Apr 2019. Submit your article to this journal View Crossmark data Full Terms & Conditions of access and use can be found at https://www.tandfonline.com/action/journalInformation?journalCode=ictx20 CLINICAL TOXICOLOGY, http://dx.doi.org/10.1080/15563650.2019.1598646 39th International Congress of the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT) 21-24 May 2019, Naples, Italy 1. Analysis of 350 consecutive cases presented dyspnea, impaired concentration, dizziness, headache and emotional lability. of carbon monoxide (CO) poisoning: Conclusion: In this case series CO poisoning usually occurred accidentally, mainly by IUB or HSM. The most frequent symptoms the Florentine experience were headache and loss of consciousness, and 69.1% of patients needed HBO. Nonetheless, one third of HBO treated patients still Anita Ecolinia, Alessandro Zottoa, Angelo Rotuloa, showed mild symptoms 1-month after discharge. Major neuro- Alessandra Ierib, Emanuela Masinia, Guido Mannaionic logical symptoms were present in patients who did not complete b HBO therapy, thus underlining the importance of HBO in order to and Francesco Gambassi avoid neurological sequelae. aDepartment of Neurofarba, University of Florence, Florence, Italy; bMedical Toxicology Unit and Poison Control Center, Azienda 2. Correlation between clinical signs Ospedaliero-Universitaria Careggi, Florence, Italy; cNeuroscience, Psychology, Drug Research and Child Health, Università degli Studi and/or symptoms and blood cyanide di Firenze, Florence, Italy concentrations in victims of cyanide Objective: CO poisoning is a leading cause of morbidity and poisoning mortality worldwide. It is mainly caused by heating system mal- function (HSM) or improper use of braziers (IUB). CO binds to Hanne Herbots, Greet Dieltiens and Kurt Anseeuw heme proteins, reducing blood oxygen transport, blocking mito- chondrial adenosine triphosphate (ATP) production, inducing cel- Emergency Medicine, ZNA Stuivenberg, Antwerp, Belgium lular anoxia and damaging the central nervous system, myocardium and muscles. Therapy is supportive, with oxygen as Objective: Diagnosis of cyanide poisoning is difficult [1,2]. We the antidote (normobaric: NBO; hyperbaric: HBO). We present a sought to identify key features in decision-making in cyanide case series of 350 consecutive patients admitted to the Azienda poisoning. Ospedaliero-Universitaria Careggi, Florence Emergency Methods: Retrospective chart review of suspected cyanide poi- Department (ED) from January 2006 to July 2018, focusing on sonings at ZNA Hospital, Antwerp, between 1 October 2013 and clinical aspects, therapy and follow up (FU). 1 October 2017. Descriptive statistics were used for demograph- Case series: Of 350 patients, 195 were female (13 pregnant) and ics, source, clinical characteristics and management. Univariate 155 male; mean age was 40 ± 20 years (range: 2 months-97 analysis was performed. Multivariate analysis was unreliable due years), 32 were <18 years. There were 172 Italians (49.1%) and to small sampling and missing data. We attempted to develop an 178 migrants (50.9%). Poisonings were caused mainly by IUB algorithm with fast and objective parameters. (151, 43.1%) and HSM (149, 42.6%), while 12 (3.4%) suicidal Results: Overall 156 patients (including 48 emergency responders from Wetteren) were included. Hydrogen cyanide was the most attempts by engine exhaust and 8 (2.3%) fire-related. At ED frequent form (n ¼ 99; 63.5%), followed by nitriles (n ¼ 54; 34.6%) admission 335 (95.7%) presented with Glasgow Coma Score and cyanide salts (n ¼ 3; 1.9%). The most common mechanism (GCS) 15, 10 (2.8%) between ≤14 and ≥10, and 5 (1.4%) ≤ 7 with was smoke inhalation (n ¼ 98; 62.8%). Descriptive analysis is seizures and vomiting. Most frequent symptoms were headache reported in Table 1. Predictors for elevated cyanide blood con- (56%), loss of consciousness (43.4%), dizziness (18.6%), nausea centrations identified by univariate analysis were smoke inhal- (17.7%), vomiting (15.7%), rhabdomyolysis (14.3%), electrocardio- ation (p ¼ 0.005), enclosed-space fire (p ¼ 0.005), rescued patient gram (ECG) abnormalities (20.9%, including cardiac ischemia pat- (p ¼ 0.02), elevated lactate (p ¼ 0.02), elevated carboxyhemoglo- tern, tachycardia, atrial fibrillation) and troponin increase (9.1%). bin (COHb) concentration (p ¼ 0.02) and elevated ethanol con- Rare events were decreased vision, postural instability, cold centration (p ¼ 0.02). Unconsciousness (p ¼ 0.01), cardiac arrest sweats, tinnitus, hoarseness and diarrhea. In total 242 (69.1%) (p ¼ 0.045), decreased bicarbonate (p ¼ 0.05) and elevated anion individuals satisfied clinical criteria for HBO in order to reduce gap (p ¼ 0.03) were predictors for blood cyanide concentrations the risk of persistent or delayed neurologic sequelae; 194 (80.1%) above 1000 µg/L. For smoke inhalation, combining lactate >2 received three or more sessions; 20 could not complete the treat- mmol/L and bicarbonate <22 mmol/L OR lactate >2 mmol/L, ment since no ear equalization could be obtained thus posing a bicarbonate 22-26 mmol/L and COHb >10% could adequately risk of eardrum barotrauma. The others received NBO until reso- identify cyanide poisoning victims. The respective positive and lution of clinical symptoms. In total, 150 (42.9%) presented for 1- negative predictive values were 88% and 95%, and 89% and month follow-up: 61 (40.7%) were still symptomatic (headache, 100%. dizziness, asthenia, impaired concentration, memory loss and Conclusion: Classical signs of cyanide poisoning (bitter almond hypoesthesia); 5 in the group that did not complete HBO therapy odor, cherry red skin) were absent in these cases. Combination of ß 2019 Informa UK Limited, trading as Taylor & Francis Group 2 ABSTRACTS Table 1. Clinical signs and treatment in patients with cyanide poisoning (n ¼ 156). Parameter Yes No Unknown Clinical signs, symptoms and observations Bitter almond odor detected 0 (0%) 156 (100%) 0 (0%) Red cherry skin 0 (0%) 156 (100%) 0 (0%) Dizziness 8 (5.1%) 148 (94.9%) 0 (0%) Vomiting 6 (3.9%) 150 (96.2%) 0 (0%) Respiratory distress 29 (18.6%) 127 (81.4%) 0 (0%) Unconsciousness/confusion 23 (14.7%) 133 (85.3%) 0 (0%) Seizures 0 (0%) 156 (100%) 0 (0%) Cardiac arrest 4 (2.6%) 152 (97.4%) 0 (0%) Sooty face 41 (26.3%) 105 (67.3%) 2 (1.2%) Burn wounds 46 (29.5%) 109 (68.9%) 1 (0.7%) Treatments and investigations Elevated ethanol concentration 29 (18.6%) 29 (18.6%) 98 (62.8%) Hydroxocobalamin given 60 (38.5%) 96 (61.5%) 0 (0%) Intubation/ventilation 58 (37.2%) 98 (62.8%) 0 (0%) Vasopressors given 29 (18.5%) 126 (80.8%) 1 (0.7%) lactate >2 mmol/L and bicarbonate >22 mmol/L or lactate >2 United States; kPostgraduate Institute of Medical Education and mmol/L, bicarbonate 22-26 mmol/L and COHb >10% could be Research, Chandigarh, India; lDepartment of Intensive Care, used to diagnose cyanide poisoning. Cliniques Universitaires Saint Luc, Université Catholique de Louvain, Brussels, Belgium; mDepartment of Acute Medicine, Ullevaal University Hospital, Oslo, Norway; nDepartment of Medical References and Toxicological Critical Care, Lariboisière Hospital, INSERM UMRS 1144, Paris-Diderot University, Paris, France; oMedical Toxicology [1] Anseeuw K, Delvau N, Burillo-Putze G, et al. Cyanide poisoning by Research Center, School of Medicine, Mashhad University of fire smoke inhalation: a European expert consensus. Eur J Emerg Medical Sciences, Mashhad, Iran; pDepartment of Pharmacology, – Med. 2013;20:2 9. University of Sydney, NSW Poison Information Center, Sydney, [2] Parker-Cote JL, Rizer J, Vakkalanka JP, et al. Challenges in the diagno- Australia; qOccupational Medicine, 1st Faculty of Medicine, Charles sis of acute cyanide poisoning. Clin Toxicol (Phila). 2018;56:609–617. University and General University Hospital, Toxicological Information Centre, Prague, Czech Republic; rAnesthesiology and ICU, Pärnu County Hospital, Pärnu, Estonia; sEmergency Medicine, 3. A consensus statement on the VSGH, Ahmedabad, India; tEmergency Medicine, Kerman University of Medical Sciences, Kerman, Iran; uClinical Biochemistry and management of patients in outbreaks Pharmacology, Tomas Bata Hospital, Zlín, Czech Republic; vAcute of methanol poisoning Medicine, The Norwegian CBRNE Centre of Medicine, Oslo University Hospital, Oslo, Norway Hossein Hassanian-Moghaddama, Nasim Zamanib, c d e Objective: The aim of our study was to develop a strategy for Darren Roberts , Jeffrey Brent , Kenneth McMartin , prioritising patients, who are being treated with alcohol dehydro- Cynthia Aaronf, Michael Eddlestong, Kent Olsonh, genase inhibitors, for haemodialysis during methanol poisoning Paul I Dargani, Lewis Nelsonj, Ashish Bhallak, outbreaks. Philippe Hantsonl, Dag Jacobsenm, Bruno Mégarbanen, Methods: Twenty-two international experts on methanol poison- Mahdi Balali-Moodo, Nicholas Buckleyp, ing were invited to join the process; consensus statements were q r s made by a