Metaldehyde is a readily available commercial pesticide, responsible for both intentional and accidental poisononing in animals. 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.
Metaldehyde intoxication is considered a rare condition that causes severe clinical signs of neurotoxicity. Currently, the World Health Organization (WHO) classifies metaldehyde as a class II toxin and therefore it can be moderately hazardous with acute toxicity, although the mechanism involved in such toxicosis remains unknown . It is estimated that once ingested metaldehyde is exposed to gastric secretions and partially converted to acetaldehyde and further oxidized into acetic acid, though the clinical relevance of this process is doubtful. Acetaldehyde may undergo enterohepatic circulation and both metaldehyde and acetaldehyde cross the blood brain barrier, resulting in severe neurotoxicity .
Patients with a history of ingestion usually present tremors, twitching, hyperpnoea, tachycardia, nystagmus, mydriasis, hypersalivation, ataxia, seizures, acidosis, hyperesthesia, diarrhea, dehydration, hyperthermia and death [2, 4, 5]. In this case, the most prominent presenting symptoms were tachypnea, stuporous mentation, systemic tremors and tonic-clonic status epilepticus. All these symptoms were consistent with previous reports of metaldehyde toxicity [2, 4, 5], although the mechanism of metaldehyde neurotoxicity is not fully understood, by it may result from both direct and indirect effects.
The present report showed that a few hours after the alleged ingestion, the patient quickly progressed to comatose state associated with metabolic acidosis. Metabolic acidosis with respiratory alkalosis has been previously reported, as metaldehyde may affect electrolyte and acid-base balances, which can cause acidosis that may also contribute to central nervous depression and hyperpnoea .
Blood samples may also reveal increase in creatine kinase (CK), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), alanine aminotransferase (ALT), bilirubin, alkaline phosphatase (ALP) and hypoglycemia . In the present report, blood samples were collected, but due to extensive hemolysis, blood count parameters were not evaluated.
There is no currently known antidote for metaldehyde toxicosis . The main goals of the treatment include prevention of metaldehyde absorption, patient stabilization, management of the neurological signs and supportive care provision . More recently, lipid emulsion therapy has shown potential in reverting severe clinical signs . In the present case, conventional therapy was installed, but the gravity of the case and evolution of clinical signs impaired the success of the treatment. Gastrointestinal decontamination with activated charcoal is often recommend , but was not performed in this case due clinical instability and the prolonged time (3 h) before veterinary care.
Death is usually caused by central nervous system depression and respiratory failure. The possible cause of death in this case was the severe neurological depression, respiratory failure and shock, as previously reported  and confirmed by pathological findings.
Necropsy findings in patients with suspected metaldehyde poisoning are not pathognomonic and very few reports present histology findings. Hemorrhage and congestion found in the brain, heart and kidneys are compatible with acute hemorrhagic or neurologic chock. Centrolobular hepatic necrosis associated with hyperemia and hemorrhage are possibly related to the potential hepatotoxic effects of metaldehyde .
In order to confirm the intoxication, samples from feces, stomach content and different organs were submitted gas chromatography analysis. Results showed the presence of metaldehyde in all samples. Previous studies have detected intact metaldehyde in gastrointestinal tract, brain, blood and liver of orally dosed mice [2, 14], but to the authors knowledge this is the first report proving the presence of this pesticide in the feces, spleen, intestines, heart and kidney of an intoxicated dog.
In most cases of metaldehyde intoxication diagnosis is made through visual inspection, clinical signs and history [2, 4, 5]. However, this is not always possible, especially when reports are incomplete and when mastication or orally administered treatments, such as activated charcoal may distort the appearance of the granules. Gas chromatography analysis of necropsy tissues, including stomach content, feces and organs may be a useful tool in the diagnosis and should be considered as a laboratory tool in postmortem cases with suspected of metaldehyde intoxication.
Other causes of acute neurological signs and extensive liver damage that were not observed in the present report include lead, strychnine, ivermectin, carbamate, organophosphate, organochlorine intoxication, tremorgenic toxins and tricyclic antidepressant acute hepatitis . These etiologies should also be considered as differential diagnoses for metaldehyde intoxication.
In conclusion, the present report describes a fatal case of metaldehyde intoxication in a dog. Clinical syndrome included tachycardia, tremors, seizures and metabolic acidosis. Pathological evaluation also revealed extensive liver damage and the presumed cause of death was neurological depression, respiratory failure and shock. To our knowledge, this is the first report proving the presence of this pesticide in feces, spleen, intestines, heart and kidney of an intoxicated dog. This report aims to contribute to the understanding of the pathogenesis of metaldehyde intoxication, to further explore veterinary forensic toxicology diagnosis.