Corine Pulce

Prevalence of anticoagulant rodenticide poisoning in humans and animals in France and substances involved

Introduction. Anticoagulant rodenticides have been used for over 50 years to control rodent populations. Since their first introduction, resistance developed in rodents, and second-generation products, more active but also more toxic, have been marketed. These compounds are currently being reviewed under European Regulations. Methods. The purpose of this work is to describe anticoagulant poisoning based on retrospective data from French human and animal poison control centers. Cases from 2004 to 2007 were collected. Results. Overall, the proportion of anticoagulant exposure reported to the Lyon poison control center appeared very limited and mostly occurred in young children, with no or very limited clinical severity. Some cases also occurred after intentional use of anticoagulants in adults. Circumstances of exposure are predominantly accidental in man (77%). In animals, both domestic and wild species, anticoagulant exposure seems more common, and often more accompanied by clinical signs. Among domestic species, dogs represent over 60% of the cases: in wildlife hares and rabbits account for almost 50% of the submitted cases, followed by predators and scavengers. Conclusion. Rodenticides involved are representative of the market share of anticoagulants, for human and domestic animal exposures. In wildlife, bromadiolone and chlorophacinone are by far the most important products, being the only ones registered for field use. There is no report of mortality in the human data, and less than 1% of all exposure cases in domestic animals were fatal.

Prothrombin time prolongation in paracetamol poisoning: a relevant marker of hepatic failure?

The association between paracetamol overdose and prolonged prothrombin time due to hepatic failure is well recognized. However, little is known of the possibility that paracetamol overdose can prolong the prothrombin time without overt hepatic failure. The few data from the literature suggest this is either due to a reduction in the functional levels of the vitamin K-dependent clotting factors by elevated doses of paracetamol, or a consequence of the administration of the antidote N-acetylcystein. The three reported cases provide further evidence that paracetamol overdose can be associated with a prolongation in the prothrombin time without overt hepatic failure. Even though the prothrombin time provides useful prognosis information, decisions regarding the management of these patients should not solely be based on this endpoint to avoid misinterpretation of the accuracy and the severity of liver failure.

Intoxication by large amounts of barium nitrate overcome by early massive K supplementation and oral administration of magnesium sulphate

Suicide by ingestion of barium is exceptionally rare. Adverse health effects depend on the solubility of the barium compound. Severe hypokalemia, which generally occurs within 2 hours after ingestion, is the predominating feature of acute barium toxicity, subsequently leading to adverse effects on muscular activity and cardiac automaticity. We report one case of acute poisoning with barium nitrate, a soluble barium compound. A 75-year-old woman was hospitalized after suicidal ingestion of a burrow mole fumigant containing 12.375 g of barium nitrate. About 1 hour post-ingestion, she was only complaining of abdominal pain. The ECG recording demonstrated polymorphic ventricular premature complexes (VPCs). Laboratory data revealed profound hypokalemia (2.1 mmol/L). She made a complete and uneventful recovery after early and massive potassium supplementation combined with oral magnesium sulphate to prevent barium nitrate absorption.

Can morels (Morchella sp.) induce a toxic neurological syndrome

Introduction.  Several cases of morel poisoning associated with neurological symptoms have been reported. The objective of this study was to describe this new mushroom poisoning syndrome. Material and methods. Retrospective study of morel poisonings collected in the French Poison Control Centers from 1976 to 2006. Cases were classified as neurological syndrome (NS; tremor or dizziness/inebriation or unsteadiness/ataxia ± associated with gastrointestinal symptoms) or isolated gastrointestinal syndrome. Results. 146 patients presented gastrointestinal syndrome (median time to onset: 5 h) and 129 presented NS (12 h) after morel consumption. Gastrointestinal (67%) and other neurological symptoms were also present (mainly ocular/vision disorders: 26%, paresthesia: 7%, drowsiness/confusion: 6%, and muscle disorders: 6%). These patients more frequently ingested a large quantity of morels. Confusion with Gyromitra was ruled out. Discussion. The NS is very different from the common gastrointestinal syndrome occurring after ingestion of poorly cooked morels and is not limited to a cerebellar syndrome.

Bone marrow aplasia following acute poisoning with chloroquine-proguanil.

Acute poisonings involving chloroquine are common in sharp contrast to those involving proguanil, another antimalarial drug. A 39-year-old woman ingested a combination of 11.2 g chloroquine and 22.4 g proguanil (i.e., 112 tablets of the commercial product Savarine®). She presented with cardiovascular disorders typically associated with chloroquine overdose, but unexpectedly bone marrow aplasia developed on day 3 post-ingestion that required granulocyte-colony stimulating factor administration, and recovered on days 10–14. Toxicological analysis evidenced both chloroquine and proguanil in the patients serum and ruled out the involvement of any major myelotoxic drug. This is seemingly the first report of bone marrow aplasia following acute poisoning with chloroquine and proguanil. The antifolinic effect of proguanil is hypothesized to have potentiated the still debated myelotoxicity of chloroquine in this patient.