Fatal metaldehyde poisoning in a dog confirmed by gas chromatography.

BACKGROUND: Metaldehyde is a toxic pesticide used mainly as a molluscicide, responsible for intoxication and deaths in both humans and animals. Accidental exposure to metaldehyde in dogs is considered rare, but severe. Data concerning clinical and veterinary forensic toxicology are largely incomplete, especially regarding case reports in dogs. The present work reports a complete and detailed description of a case from the history, clinical evolution, pathological exams and toxicological diagnosis in an accidental case of metaldehyde poisoning in dog. CASE PRESENTATION: An eleven-month-old, 3.0 kg, male German Spitz was presented for emergency care with acute vomiting and seizures 3 hours after suspected accidental ingestion of commercial molluscicide containing 3% metaldehyde (Lesmax®). The animal was in lateral recumbency and showed stuporous mentation, salivation, tonic-clonic status epilepticus, systemic tremors, bilateral miosis, absent palpebral, corneal, oculovestibular and gag reflexes, severely depressed spinal reflexes, dyspnea and tachycardia. Despite treatment, the patient progressed to comatose mentation and died. Necropsy examination revealed discrete lesions in the liver and central nervous system, while stomach examination revealed content of feed, activated charcoal and blue-green granules, compatible to the commercial formula of metaldehyde. Histology examination revealed extensive hemorrhage and severe centrolobular necrosis of the liver and tumefaction of Kupfer cells. Brain samples showed discrete hemorrhage and hyperemia. In order to confirm the diagnosis, samples from feces, stomach content, spleen, liver, heart, kidneys and brain were submitted gas chromatography analysis. Results confirmed the presence of metaldehyde in all samples. We describe clinicopathological abnormalities of a fatal case of metaldehyde poisoning in a dog, as well as postmortem diagnosis using gas chromatography. CONCLUSION: Metaldehyde poisoning is rarely reported, since the diagnosis is often difficult and the notifications scarce. To our knowledge, this is the first report describing clinical signs, pathological findings and chromatographic diagnosis. This report aims to contribute to the understanding of the pathogenesis of metaldehyde intoxication, to further explore veterinary forensic toxicology diagnosis.

Super-refractory nonconvulsive status epilepticus due to self-poisoning with metaldehyde.

INTRODUCTION: Metaldehyde self-poisoning in adults is uncommon and, to the best of our knowledge, an episode of super-refractory nonconvulsive status epilepticus (sr-NCSE) following an suicide attempt has not been previously demonstrated. CASE REPORT: A 68-year-old woman was admitted to our Intensive Care Unit (ICU) in coma. On neurologic examination, the pupils were reactive, brainstem reflexes were present and plantar responses were flexor bilaterally. Routine laboratory tests were unremarkable. Arterial blood gas analysis revealed a mixed acidosis. A computed tomography (CT) scan of the brain and angio-CT were normal. The family confirmed that the patient had had suicidal ideation, and they had discovered a bag of slug killer (metaldehyde 5%) in her room. Two hours after the admission at the ICU, her neurological state remained unchanged. Sedation with intravenous propofol and antiepileptic therapy with levetiracetam (1000 mg/24 h) were started. The next day, propofol infusion was stopped but the level of consciousness of the patient did not improve. A video-electroencephalograhy (v-EEG) showed continuous generalized paroxysms of spike-wave and sharp-slow wave complexes compatible with the diagnosis of generalized NCSE. On day 3, the episode of NCSE was controlled. Finally, 15 days after ICU admission she was discharged with a normal neurological examination. CONCLUSION: This clinical case highlights that in comatose patients as consequence of metaldehyde poisoning, a v-EEG evaluation should be perform in order to rule out the existence of NCSE.

Suspected metaldehyde slug bait poisoning in dogs: a retrospective analysis of cases reported to the Veterinary Poisons Information Service.

A retrospective analysis of telephone enquiries to the Veterinary Poisons Information Service found 772 cases with follow-up concerning suspected metaldehyde slug bait ingestion in dogs between 1985 and 2010. Half the enquiries occurred in the summer months. The amount and strength of the slug bait ingested was rarely known. In 56, cases the quantity consumed was estimated and was on average 229.6 grams of bait. Clinical signs developed in 77.3 per cent of dogs; common signs were convulsions, hypersalivation, twitching, hyperaesthesia, tremor, vomiting, hyperthermia and ataxia. Only 4.6 per cent of dogs developed hepatic changes, and only one developed renal impairment. The average time to onset of signs was 2.9 hours post-ingestion, with 50.3 per cent of dogs developing effects within one hour. Increased muscle activity (twitching, convulsions) lasted on average 15.2 hours. Recovery time was reported in 61 cases and occurred on average at 39.3 hours. Common treatments were gut decontamination, anticonvulsants, anaesthetics and intravenous fluids. Of the dogs that were treated with sedatives, 45.8 per cent required more than one sedative or anaesthetic agent. Methocarbamol was rarely used, probably due to unavailability. The outcome was reported in 762 dogs; 21.7 per cent remained asymptomatic, 61.7 per cent recovered and 16 per cent of dogs died or were euthanased. Where known (only six cases), the fatal dose of bait ranged from 4.2 to 26.7 g/kg (average 11.8 g/kg).

Effect of prolonged status epilepticus as a result of intoxication on epileptogenesis in a UK canine population.

The aim of the present study was to investigate if prolonged status epilepticus (SE), secondary to a chemoconvulsant, can induce spontaneous recurrent seizures in dogs. Clinical records at two UK referral hospitals were searched for dogs that presented in SE secondary to intoxication. Dogs were only included in the study if there was clear historical evidence of intoxication and a prolonged SE. Clinical and follow-up information was retrieved and verified by using a combination of clinical records from the two hospitals and the referring veterinarian and by contacting the owners using a telephone questionnaire. Twenty dogs met the inclusion criteria: 17 presented for metaldehyde toxicity, one for moxidectin toxicity, one for theobromine toxicity and one for mycotoxin toxicity. Of these 20 dogs, three dogs had an SE duration between 0.5 and one hour, four dogs between one and 12 hours, 10 dogs between 12 and 24 hours and three dogs greater then 24 hours. Median follow-up time for the 20 dogs was 757 days (range 66 to 1663 days). No dog had any further seizures after its SE. The present study supports the view that dogs with a prolonged SE following intoxication with the aforementioned toxins might not need long-term treatment with antiepileptic drugs after the SE has been controlled.

Determination of metaldehyde in human serum by headspace solid-phase microextraction and gas chromatography-mass spectrometry.

A rapid headspace solid-phase microextraction-gas chromatography-mass spectrometry (HS-SPME-GC-MS) method has been developed for the determination of metaldehyde in human serum samples. Metaldehyde is extensively used as a molluscicide for the control of slugs and snails, and cases of metaldehyde poisoning have been reported. Metaldehyde was headspace-extracted on a polydimethylsiloxane (PDMS) fiber at 70 degrees C for 25 min, desorbed, and analyzed rapidly by GC-MS. The method was validated for limit of detection (LOD), linearity, precision, and recovery. Although the recovery of the sample was very low, the method itself was rapid with a low detection limit of 0.25 microg/ml, R.S.D. value 12.6%, and linearity range 0.5-25.0 microg/ml (r(2)=0.999). The results demonstrated that the SPME-GC-MS method for the analysis of metaldehyde is simple, rapid, solvent-free, and does not require any pre-analysis conversions.

Clinical, neurological and clinicopathological signs, treatment and outcome of metaldehyde intoxication in 18 dogs.

OBJECTIVES: To describe the clinical signs, clinicopathological abnormalities and outcome of metaldehyde intoxication in dogs. METHODS: Medical records of dogs presenting between 1989 and 2005 with a diagnosis of metaldehyde toxicity were reviewed retrospectively. Data obtained from the medical record included signalment, history, clinical signs, laboratory tests results, hospitalisation period length, treatments and outcome. RESULTS: Eighteen dogs fulfilled the inclusion criteria. The most prevalent clinical signs were seizures, hyperthermia, tachycardia and muscle tremors. Serum biochemistry abnormalities included increased serum muscle enzymes activities, acidaemia (six dogs) and decreased blood bicarbonate (eight dogs). Treatment was symptomatic and supportive. Hyperbilirubinaemia was observed in two dogs. Diazepam was the most commonly used anticonvulsant followed by phenobarbitone and pentobarbital. General inhalant anaesthesia was required in nine of 18 dogs with seizures unresponsive to anticonvulsants. The survival was 83 per cent (15 of 18 dogs). CLINICAL SIGNIFICANCE: This clinical study recorded, for the first time in the veterinary literature, several clinicopathological abnormalities from severely intoxicated dogs. Metabolic acidosis was common, while acute or delayed hepatotoxicity was an uncommon complication.

Acute metaldehyde poisoning in Taiwan.

Metaldehyde, a cyclic tetramer of acetaldehyde, is a widely used molluscicide. Although cases with acute metaldehyde poisoning have been reported, the occurrence of severe poisoning is uncommon. To provide more information on human metaldehyde poisoning, we reviewed 15 cases of metaldehyde exposure reported to the Taiwan National Poison Control Center at the Taipei Veterans General Hospital between 1991 and 2002. While 7 patients were asymptomatic, the other 8 patients, including 4 who coingested alcohol or other poisons, exhibited toxic manifestations of abdominal pain, dizziness, nausea, irritation of oral mucosa, and seizures after oral exposure. One patient died after ingesting 12 g (or 258.6 mg/kg) of metaldehyde. Although the toxicity from metaldehyde is largely mild, the clinical course of metaldehyde poisoning may be rapidly deteriorating and fatal on rare occasions. Physicians should therefore be cautious in managing patients with metaldehyde poisoning, and vigorous supportive measures should be promptly instituted in patients who manifest severe toxicity.

[Case report-fatal snail bait (metaldehyde) overdose presenting aspiration pneumonia].

A-55-year-old man ingested unknown amount of snail poison bait containing metaldehyde. He was mentally retarded and presented pica. On admission, his vital sign was stable, and the extremeties were spastic. Then, gastric lavage was unsuccessful because of massive unbited food. Activated charcoal and cathartic were administrated. On the next day, general convulsion occurred and respiratory distress advanced, so he was intubated. On the 3rd day, infiltration shadow appeared on chest roentogenogram and, his respiration was assisted mechanically. Thereby, acute lung injury advanced regardless of tracheostomy, kinetic therapy, antibiotics and steroid pulse therapy. He died of respiratory failure on the 33rd day. Serum test showed HBs and HBe antigen, CT scan revealed ascites and splenomegaly; the clinical course might be worsened by liver cirrhosis. HPLC revealed metaldehyde in the serum (total 80.6 microg/ml). He ingested 2.7 g of metaldehyde maximally estimated. Although Japan Poison Information Center reported that snail poison bait poisoning is often in dogs in Japan, human poisoning is rare.

Pesticide toxicosis in the horse.

Toxicosis from pesticides rarely occurs in horses and is usually the result of inappropriate pesticide use or handling by humans. Organophosphorus and carbamate insecticides inhibit acetylcholinesterase and are the insecticide class most frequently associated with toxicosis in domestic animals. Metaldehyde is a molluscicide, and zinc phosphide is a rodenticide, both of which have caused toxicosis in horses. All three of these pesticides affect the nervous system of horses and can be fatal if not treated promptly.

[Pesticide poisoning]. / Intoxications par produits agricoles.

Pesticide intoxications are mainly accidental with a benign course, such as ingestions of diluted fertilizers or low concentration antivitamin K rodenticides, ant-killing products or granules of molluscicides containing 5% metaldehyde. Voluntary intoxications by chloralose, strychnine, organophosphorus or organochlorine insecticides, concentrated anti-vitamin K products, herbicides such as paraquat, chlorophenoxy compounds, glyphosate or chlorates may be severe. Toxicity is due to active substances but also to solvents or surfactants included in the composition. Analysis done in a toxicology laboratory help in establishing diagnosis, prognosis and treatment. Poison centres may be called constantly to help for the evaluation of these intoxications.

Persistence of metaldehyde during acute molluscicide poisoning.

A case is presented in which a 37-year-old man took an overdose of Slugit, liquid containing metaldehyde. Significant concentrations were found in his serum and urine for several days afterwards. Acetaldehyde and ethanol were not detected. The significance of these findings is discussed.