Exposures associated with making or playing with viscoelastic polymer toys known as Slime: a retrospective case series from French Poison Control Centres.

Context: Slime is a slow-flowing material with viscoelastic properties which is attractive to children. Its preparation is based on the crosslinking of polyvinyl alcohol, polyvinyl acetate or starch with boric acid.Objectives: The goal of this study was to describe the adverse effects of Slime.Materials and methods: This is a descriptive retrospective study of cases of exposure reported to French Poison Control Centres between January 2014 and May 2018. The following parameters were used: age and sex, date and circumstances of exposure, symptoms and severity.Results: Two hundred and eight (208) cases of exposure were recorded, 93 cases happened in 2017, and 88 cases in the first four and a half months of 2018. The average age was of 8 years old; 190 patients were younger than 15. Fifty-seven percent (57%) were female. Regarding routes of exposure, 168 were oral, 30 cutaneous, eight ocular, one inhalation and one ear exposure. Eighty-two (82) patients were symptomatic, including 81 cases of low severity and one of average severity (keratitis). All cases lead to recovery.Conclusion: No significant adverse health effects are expected to develop if only small amounts are swallowed; making Slime with home ingredients is a potential cause of boric acid exposure that must be supervised by adults.

European viper envenomation recorded by French poison control centers: A clinical assessment and management study.

INTRODUCTION: Immunotherapy is the gold standard treatment for patients bitten by European vipers in France; it significantly decreases morbidity, frequency and severity of complications and length of stay. A national prospective study was performed by all Poison Control Centers (PCC) to validate the emergency protocol for viper envenomations. METHODS: This prospective study included all cases of viper bites in France, treated or not with Viperfav(®) in 2013. RESULTS: In 2013, 277 cases of viper bites were collected: ratio M/F 2.1; mean aged 43 years (<15 years 25% 15-65 63% > 65 12%). The final severity was divided into 68 grades 0, 58 grades I, 62 grades IIA, 71 grades IIB and 18 grades III. One death was reported. Five patients had neurological signs. For the 114 patients who received Viperfav(®), all systemic signs disappeared in 5 h and in 24 h for biological and neurological signs. No severe anaphylactic reaction with Viperfav(®) was reported. Late Viperfav(®) administration increased the risk of functional impairment 15 days after the bite (OR = 3.21 p = 0.043). The administration of Low Molecular Weight Heparin (LMWH) increased the frequency of functional impairment to 15 days after the bite (OR = 6.38 p = 0.064), although Viperfav(®) was given in the first 18 h. DISCUSSION: This study confirms the efficiency, safety and recommendation of an early administration of a single dose of Viperfav(®), LMWH should not be used. It also shows the extension of neurotoxic venom of vipers in France.

Chlormequat poisoning is not without risk: Examination of seven fatal cases.

Chlormequat chloride is a plant growth regulator. Chlormequat poisoning clinically resembles anticholinesterase insecticide poisoning. The cholinergic symptoms result from direct action on nicotinic and muscarinic receptors and not from inhibition of the cholinesterase activity. This case series confirms the extreme gravity of chlomequat poisoning with a risk of death in the hour following ingestion.

[Sodium dichloroisocyanurate-induced acute lung injury in a child]. / Œdème pulmonaire lésionnel par intoxication au dichloro-isocyanurate de sodium.

Intoxication, by cyanurate and its chlorated derivatives in children, is increasingly reported in the literature due to accidental ingestion compared to accidental inhalation. We report a case in a 5-year-old child who presented with acute lung injury due to accidental inhalation of gas formed after a reaction of sodium dichloroisocyanurate tablets with water. Prevention remains the best way to reduce the risk of children being intoxicated by inhalation of the gas formed after contact of tablets with water.

[Pediatric poisoning with triptans: review of cases in the Lille poison center between 2000 and 2010]. / Intoxications pédiatriques par les triptans : revue des cas recensés au centre antipoison de Lille (2000-2010).

BACKGROUND AND OBJECTIVE: Triptans are recommended to treat acute migraine. Pediatric data remain insufficient for making decisions in cases of triptan poisoning. Consequently, hospitalization is often warranted as a precautionary measure. This study aims to more accurately estimate the risks incurred when a young child ingests triptan tablets. MAIN OUTCOME MEASURES: This study reviewed all cases of acute triptan poisoning listed by the Lille poison center between January 2000 and December 2009 in children younger than 6 years. Cases with certain ingestion, no drug interactions, and no other known etiology were selected. The gravity of each case was estimated by the poisoning severity score and follow-up was conducted by phone. RESULTS: A cohort of 84 patients was collected: 6% were lost to follow-up. The mean intake was 1.22 tablets (range, 0.25-6), for the most part zolmitriptan (64.2%), eletriptan (14.3%) and naratriptan (14.3%). Fifty-nine children (74.5%) were admitted to the hospital and 20 children monitored at home. The majority received evacuation or adsorbing treatment. Symptoms were not frequent (13%) and were well tolerated, in particular on the hemodynamic level (ten cases of PSS1). The adverse events observed were tachycardia (4 cases), arterial hypertension (1 case), dyspnea (2 cases), drowsiness (2 cases), marbling of the extremities (1 case), vomiting (3 cases), and digestive pain (1 case). The 2 cases of dyspnea, induced by 2.5mg and 7.5mg of zolmitriptan, respectively, were associated with cardiovascular symptoms and were left untreated. According to its pharmacological action, the potential risk of a serotoninergic syndrome is a concern with triptan intake. No severe complication was recorded, so based on this study, our guidelines were updated. The response should be less alarmist, but a watchful attitude should be retained. Hospitalization should not be systematic, but focused on the patient's cardiac history, the dose, and the symptomatology. If the child remains at home, specific action should be managed: an adsorbing treatment and close monitoring by phone remain essential.

Torsade de pointes: a severe and unknown adverse effect in indoramin self-poisoning.

We report the two first cases of torsade de pointes associated with QT interval prolongation following a large ingestion of indoramin.

[Accidental ingestion of methadone and buprenorphine by children. A case review of the Lille Poison Centre between 1995 and 2005]. / Ingestions accidentelles de produits de substitution par des enfants. Revue des cas du centre antipoison de Lille 1995-2005.

We have performed a retrospective study (1995-2005) on 218 accidental intoxications in children less than 15 years old, linked to drugs used in the management of opiate withdrawal (cases registered at the Lille poison centre) This study shows a peak of frequency in children less than 3 years old, with a predominance of boys. Poisonings with buprenorphine are more frequent but ingestions of methadone are often more severe (p = 0.004).

[Fatal poisoning caused by the ingestion of a concentrated solution of 2,4-D and MCPP]. / Ingestion mortelle d'une solution concentree de 2,4-D et de MCPP.

We report a clinical case of lethal ingestion of an herbicide containing 100 g/L of 2,4-D and 400 g/L de MCPP. The patient shows quickly disturbances of consciousness and cardiac arythmy, a severe metabolic acidosis and an hyperkalemia. The digestive endoscopy at day 4 after ingestion shows an haemorrhagic mucous membrane at oesophagus and stomach level with numerous aulcerations. The bronchial endoscopy shows an inflammatory mucous membrane covered with haemorrhagic liquid. At day 6, appearance of a toxic medullar aplasia. The patient dies at day 7. the autopsy shows haemorrhagic digestive lesions, a bilateral pneumopathy, lungs oedema, an ascite but no cerebral oedema.

[Biomarkers for toxicity and metabolic abnormalities of the main severe poisonings. Clinical and toxicologic symptoms. Conservative determination]. / Biomarqueurs de toxicité et anomalies métaboliques dans les principales intoxications graves. Symptomatologie clinique et toxique. Le prélèvement conservatoire.

The members of the joint group "Toxicology and Clinical Biology" of the French Society of Clinical Biology (SFBC), the French Society of Analytical Toxicology (SFTA), and the Society of Clinical Toxicology (STC), suggest guidelines to meet the requirements of clinical biologists who are not specialized in toxicology. Based on good laboratory practice they propose a number of guidelines. Three synthetic tables have been established. They are not only toxicity biomarkers and metabolic disorders associated with the main severe intoxications, but also clinical signs that are observed during these intoxications, finally biological sampling as a precautionary measure. The table also takes into account approximately fifty xenobiotics: main clinical signs emergency, identification or quantification of the suspected product, useful biological markers, therapeutic, quantitations necessary to take into consideration patient care, and poison antidotes, are described. Recommendations regarding medical and forensic techniques are also proposed by the group. It is also necessary to collect and store biological samples when the individual patients are in charge. These samples will be analyzed or not depending on the individual case history.

[Aldicarb poisoning: review of cases in the North of France between 1998 and 2001]. / Intoxications par l'Aldicarbe: revue des cas survenus dans le Nord de la France entre 1998 ET 2001.

Among the 2,726 cases of human pesticide poisoning collected at the Poison Centre of Lille from January 1998 to May 2001, 39 cases were related to the ingestion of aldicarb. Analysis of the circumstances found a suicide attempts in 33 cases and an accidental ingestion in 6 cases. The sex-ratio was 31 men for 8 women, mean age was of 36.6 years (15 months--77 years). Thirty one poisoning were symptomatic with muscarinic signs (20 cases), digestive (15 cases), neurological (8 cases), nicotinic signs (6 cases). Treatment was based on digestive evacuation (14 cases), administration of activated charcoal (14 cases), atropine (7 cases), pralidoxime (1 case), preservative vital functions by intubation and ventilation (7 cases). Sedation was necessary in 4 cases. Hospitalization was necessary in 34 cases. The Poison Severity Score was estimated at 0 (any gravity) in 5 cases, 1 (weak) in 12 cases, 2 (moderate) in 7 cases, 3 (severe) in 8 cases and 4 (lethal) in 2 cases. In one of deaths, aldicarb was determined by HPLC-DAD in blood (6.04 micrograms/ml), urines (1.88 micrograms/ml) and gastric contents (3.98 micrograms/ml). These concentrations are the most important ever described in the literature. Aldicarb is the most toxic carbamate insecticide for human.

[Fatal intoxication after accidental ingestion of viscous 2% lidocaine in a young child]. / Intoxication mortelle après ingestion accidentelle de xylocaine visqueuse à 2% chez une jeune enfant.

We report a case of fatal intoxication with 2% viscous lidocaine. A 18 month old infant was admitted after malaise and cardiorespiratory arrest at home. He was resuscitated, then seizures appeared before arrival at the hospital. Treatment was symptomatic, including cardiorespiratory resuscitation and administration of anticonvulsants. Identification of lidocaine and its metabolite monoethylglycinexylidide (MEGX) MEGX was performed after organic extraction by High Performance Liquid Chromatography (HPLC) with Diode Array Detection (DAD); the serum concentrations, determined by Fluorescence Polarisation Immuno Assay (FPIA), were: 1.1 micrograms/ml for lidocaine and 0.94 microgram/ml for MEGX (H + 7) and 0.30 microgram/ml for the lidocaine (Day + 1). Neurotoxic manifestations appear at lower concentrations than cardiotoxic symptoms which are correlated with plasma levels of lidocaine. The toxic symptoms begin with headache, hallucinations, seizure, coma, respiratory arrest and circulatory collapse. The toxic symptoms can persist even after the decrease of lidocaine concentration under therapeutic levels. There is no antidote and acute lidocaine toxicity is managed with supportive therapy (diazepam for seizures, intubation, chronotropic agents). Considering the gravity of these poisonings which remain rare, the 2% viscous lidocaine prescription is forbidden for children under 6 years old.

[Serial determination of crimidine by HPLC/SE/SM in a patient ingesting a "mouse trap"]. / Détermination sérique de la crimidine par CLHP/ES/SM chez un patient ayant ingere un "souricide foudroyant".

Crimidine (2 chloro, 4 methyl, 6 dimethyl amidopyrine) is a synthetic rodenticide which causes acute poisonings after oral ingestion in human. Major toxic effects are consciousness disorders, hypertonic coma and convulsions. Toxic level in human is about 5 mg/Kg. An intoxication case is reported. Five serums collected at different times were analyzed with HPLC/ES/MS. Crimidine was extracted with ethylacetate with recovery over 80%. Linearity was up to 800 micrograms/L. LOQ and LOD were 0.5 and 0.3 microgram/L respectively. The coefficients of variation were less than 10% for repeatability and reproductibility. Serum levels varied from 368 micrograms/L for H0 to 64 micrograms/L for H10 and elimination of crimidine was linear in time.

Determination serique de la crimidine par clhp/es/sm chez un patient ayant ingere un « souricide foudroyant ¼.

Crimidine (2 chloro, 4 methyl, 6 dimethyl amidopyrine) is a synthetic rodenticide which causes acute poisonings after oral ingestion in human. Major toxic effects are consciousness disorders, hypertonic coma and convulsions. Toxic level in human is about 5 mg/Kg. An intoxication case is reported. Five serums collected at different times were analyzed with HPLC/ ES/MS. Crimidine was extracted with ethylacetate with recovery over 80 %. Linearity was up to 800 µg/L. LOQ and LOD were 0.5 and 0.3 µg/L respectively. The coefficients of variation were less than 10 % for repeatability and reproductibility. Serum levels varied from 368 µg/L for H0 to 64 µg/L for H10 and elimination of crimidine was linear in time.

Intoxications par l'aldicarbe : revue des cas survenus dans le nord de la france entre 1998 et 2001.

Among the 2 726 cases of human pesticide poisoning collected at the Poison Centre of Lille from January 1998 to May 2001, 39 cases were related to the ingestion of aldicarb. Analysis of the circumstances found a suicide attempts in 33 cases and an accidental ingestion in 6 cases. The sex-ratio was 31 men for 8 women, mean age was of 36,6 years (15 months - 77 years). Thirty one poisoning were symptomatic with muscarinic signs (20 cases), digestive (15 cases), neurological ( 8 cases), nicotinic signs (6 cases). Treatment was based on digestive evacuation (14 cases), administration of activated charcoal (14 cases), atropine (7 cases), pralidoxime (1 case), preservative vital functions by intubation and ventilation (7 cases). Sedation was necessary in 4 cases. Hospitalization was necessary in 34 cases. The Poison Severity Score was estimated at 0 (any gravity) in 5 cases, 1 (weak) in 12 cases, 2 (moderate) in 7 cases, 3 (severe) in 8 cases and 4 (lethal) in 2 cases. In one of deaths, aldicarb was determined by HPLC-DAD in blood (6,04 µg / ml), urines (1,88 µg / ml) and gastric contents (3,98 µg / ml). These concentrations are the most important ever described in the litterature. Aldicarb is the most toxic carbamate insecticide for human.

Intoxication mortelle après ingestion accidentelle de xylocaine visqueuse à 2% chez une jeune enfant.

We report a case of fatal intoxication with 2% viscous lidocaine. A 18 month old infant was admitted after malaise and cardiorespiratory arrest at home. He was resuscitated, then seizures appeared before arrival at the hospital. Treatment was symptomatic, including cardiorespiratory resuscitation and administration of anticonvulsants. Identification of lidocaine and its metabolite monoethylglycinexylidide (MEGX) MEGX was performed after organic extraction by High Performance Liquid Chromatography (HPLC) with Diode Array Detection (DAD); the serum concentrations, determined by Fluorescence Polarisation Immuno Assay (FPIA), were : 1,1 µg / ml for lidocaine and 0,94 µg / ml for MEGX (H+7) and 0,30 µg / ml for the lidocaine (Day+1). Neurotoxic manifestations appear at lower concentrations than cardiotoxic symptoms which are correlated with plasma levels of lidocaine. The toxic symptoms begin with headache, hallucinations, seizure, coma, respiratory arrest and circulatory collapse. The toxic symptoms can persist even after the decrease of lidocaine concentration under therapeutic levels. There is no antidote and acute lidocaine toxicity is managed with supportive therapy (diazepam for seizures, intubation, chronotropic agents). Considering the gravity of these poisonings which remain rare, the 2% viscous lidocaine prescription is forbidden for children under 6 years old.

Flumazenil use in an emergency department: a survey.

OBJECTIVE: To evaluate the efficacy of flumazenil use by a one-year survey of practice in tan emergency department. DESIGN: During a one-year period, an observational prospective study in the emergency department of an urban community hospital enrolled every patient admitted with a history of pure or mixed benzodiazepine acute poisoning. Case records were secondarily reviewed by an expert group. Actual flumazenil use during hospitalization was compared to currently recommended indications. In order to evaluate the efficacy of flumazenil use, patients who received flumazenil were matched with those who did not and effects on mortality, morbidity, number of costly procedures (CT scan, diagnostic toxicology, etc.) and duration of hospital stay were determined. RESULTS: Of the 1529 patients admitted in 1 year for acute poisoning, 478 reportedly ingested at least one benzodiazepine. Twenty-nine patients (6%) received flumazenil in the emergency department whereas the expert reviewers recommended flumazenil use in only 18 (3.7%). In 11/29 (38%) cases, the use of fumazenil was considered inappropriate. The expert group considered flumazenil to be contraindicated in 93 of 478 patients. Nonetheless, flumazenil was used in 11 patients (rate of potentially harmful flumazenil use: 11/93; 12%), and a severe complication occurred in one of these patients after flumazenil. No significant difference could be shown in outcome, complication rate, number of complex procedures or duration of hospital stay between patients who received flumazenil and matched patients who did not. CONCLUSION: The use of flumazenil in the clinical practice of an emergency department fails to show any beneficial effect in adult patients. Moreover, contraindications are frequently overlooked and this may expose patients to substantial risk of complications.

Intermediate syndrome with delayed distal polyneuropathy from ethyl parathion poisoning.

An acute poisoning in a 44-y-old female who ingested 50 ml of ethyl parathion concentrate (25 g) is described. She was treated by gastric lavage, administration of pralidoxime and atropine, and mechanical ventilation. As signs of intoxication disappeared at day 3, treatment was discontinued. The patient had a relapse of acute cholinergic crisis at day 4, and the same treatment was applied again. The acute poisoning phase was followed by an intermediate syndrome and delayed distal polyneuropathy. The clinical course of this severe ethyl parathion poisoning was favorable after 40 d.