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.

[Ten practical issues concerning acute poisoning with carbon monoxide in pregnant women]. / Dix questions pratiques concernant l'intoxication aiguë au monoxyde de carbone chez la femme enceinte.

BACKGROUND: The poisoning of carbon monoxide (CO) is the leading cause of death by poisoning in France. Its consequences are potentially serious to the fetus. Literature is ancient and little known. PURPOSE AND METHOD: Make an inventory of knowledge about carbon monoxide poisoning during pregnancy. RESULT: The CO causes maternal then fetal tissue hypoxia primarily by binding to hemoglobin with which it has a high affinity. Its transplacental passage may cause fetal harm, predominantly in the brain. Severity seems correlated with maternal symptoms during exposure. In the absence of maternal symptoms, however, the available data are reassuring. Hyperbaric oxygen therapy may reduce the risk to the fetus. DISCUSSION: Oxygen therapy should be offered in all cases of CO poisoning, especially if there are maternal symptoms during exposure. In addition, a fetal echography directed on the cephalic pole - even a fetal magnetic resonance imaging three weeks after exposure - should also be proposed.

[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.

[What public health measures could reduce antenatal exposure to tobacco and improve the quality of perinatal care: the gynecologist-obstetrician's point of view]. / Quelles sont les mesures de santé publique susceptibles de réduire l'exposition anténatale au tabac et d'améliorer les indicateurs de qualité des soins périnatals? Le point de vue du gynécologue-obstétricien.

The progression of addiction to smoking among young women is particularly alarming. The fatal effects of the nicotine-poisoning on the pregnancy and on the child constitute a serious public health issue. For young women, the period of maternity plays an essential educational role. Contact with medical care during pregnancy offers a special opportunity to establish a sound basis for health. Clinicians must strive to help women become fully aware of the fatal effects of smoking, providing methods and support for abstinence through a global, structured strategy of health care. The "Maternity without tobacco" network was developed to achieve these objectives. Expired CO analysis can be an interesting tool to search for active or passive addiction to smoking, and more generally carbon monoxide poisoning.

[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.

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.

Accidental subcutaneous injection of elemental mercury. A case report.

Subcutaneous injection of elemental mercury is a very rare situation. The authors report the case of a 31-year-old man who accidentally injected an unknown quantity of metallic mercury into his left forearm. Several surgical procedures were required to reduce the blood and urinary levels of mercury. However, the patient never developed clinical signs of chronic poisoning. This observation confirms the lower risk of acute or chronic poisoning in subcutaneous injection of mercury and the need for early excision of contaminated tissue.

Carbon monoxide poisoning--a public health perspective.

Carbon monoxide (CO) may be the cause of more than one-half of the fatal poisonings reported in many countries; fatal cases also are grossly under-reported or misdiagnosed by medical professionals. Therefore, the precise number of individuals who have suffered from CO intoxication is not known. The health effects associated with exposure to CO range from the more subtle cardiovascular and neurobehavioral effects at low concentrations to unconsciousness and death after acute or chronic exposure to higher concentrations of CO. The morbidity and mortality resulting from the latter exposures are described briefly to complete the picture of CO exposure in present-day society. The symptoms, signs, and prognosis of acute CO poisoning correlate poorly with the level of carboxyhemoglobin (COHb) measured at the time of hospital admission; however, because CO poisoning is a diagnosis frequently overlooked, the importance of measuring COHb in suspicious settings cannot be overstated. The early symptoms (headache, dizziness, weakness, nausea, confusion, disorientation, and visual disturbances) also have to be emphasized, especially if they recur with a regular periodicity or in the same environment. Complications occur frequently in CO poisoning. Immediate death is most likely cardiac in origin because myocardial tissues are most sensitive to the hypoxic effects of CO. Severe poisoning results in marked hypotension, lethal arrhythmias, and electrocardiographic changes. Pulmonary edema may occur. Neurological manifestation of acute CO poisoning includes disorientation, confusion, and coma. Perhaps the most insidious effect of CO poisoning is the development of delayed neuropsychiatric impairment within 2-28 days after poisoning and the slow resolution of neurobehavioral consequences. Carbon monoxide poisoning during pregnancy results in high risk for the mother by increasing the short-term complication rate and for the fetus by causing fetal death, developmental disorders, and chronic cerebral lesions. In conclusion, CO poisoning occurs frequently; has severe consequences, including immediate death; involves complications and late sequelae; and often is overlooked. Efforts in prevention and in public and medical education should be encouraged.

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.

Gamma butyrolactone poisoning and its similarities to gamma hydroxybutyric acid: two case reports.

Clinical experience with toxicity induced by products containing gamma butyrolactone is limited. We report here 2 cases of gamma butyrolactone poisoning with a nail polish remover labelled "acetone-free". Rapid onset of coma, respiratory depression and bradycardia occurred in both patients. After supportive care, they fully recovered within a few hours.