Aluminium intoxication in a dog

Summary

A two‐year‐old male Barsoi dog was presented after a two‐week period of muscle twitching and convulsions during exercise, which worsened to a state of tetraparesis and coma. Removal of a gastric foreign body, containing aluminium, resolved the presenting signs. Parallel with this clinical recovery the elevated serum levels of aluminium decreased to values of two normal control dogs, suggesting that the neurological signs were due to A1 intoxication.     

Metaproterenol intoxication in a dog

Intoxication with metaproterenol, a mainly beta-2 selective agonist, was diagnosed in a dog with tachycardia, tachypnea, weakness, vomiting, and a history of exposure to the drug. Electrocardiography and echocardiography disclosed sinus tachycardia with episodes of ventricular tachycardia and exuberant systolic ventricular function, respectively. Administration of the beta blocking drugs propranolol and atenolol led to resolution of the clinical signs. Excessive sympathetic stimulation caused by metaproterenol is an unusual intoxication in dogs.     

Clozapine intoxication in a dog

Intoxication with clozapine in a dog, suspected from history and clinical signs at presentation, was confirmed by demonstration of decreasing serum levels of this drug. Clozapine is a tricyclic dibenzodiazepine used for treatment of human schizophrenia, and clinical signs of intoxication in humans include tachycardia, seizures, muscle fasciculations, agitation, and sialorrhea. This dog showed ptyalism, hyperthermia, tachycardia, and was easily excited by tactile or auditory stimulation. The calculated peak concentration of clozapine in this dog was approximately 6,000 ng/mL, and the elimination half-life (t(1/2)) was 5 hours. Charcoal administration and supportive care led to a successful outcome in this patient.     

Thallium intoxication in a dog

A fatal case of thallium poisoning was described in a dog. Clinical signs included vomiting, gastroenteritis, and dermal lesions. Chemical analysis of urine, liver, and kidney from the dog revealed 98, 7, and 34 ppm thallium, respectively, on a wet-weight basis.     

Milbemycinoxime intoxication in a Miniature Australian Shepherd dog

A 3-year-old female intact Miniature Australian Shepherd presented with convulsive status epilepticus after milbemycinoxime administration in the recommended dosage. In addition to continuous intravenous antiepileptic therapy the dog had to be ventilated for 36 hours due to aspiration pneumonia. After extubation control of intermittent tonic-clonic seizures required a constant-rate-infusion of propofol for another 96 hours, before it could be discontinued on day 5. The patient had fully recovered by day 10. The dog was known to be homozygous for the MDR1-gene mutation. So far milbemycinoxime was regarded a save drug in MDR1-deficient dogs. However, the present case suggests using the lowest possible dosage in MDR1-deficient dogs and pet owners should be advised of potential complications.     

Successful treatment of severe salt intoxication in a dog

Objective: To report successful treatment of severe salt intoxication and hypernatremia in a dog. Case summary: A 5‐year‐old intact female Doberman Pinscher was admitted to the intensive care unit with a history of seizures and coma. The owner had administered approximately 100 g of cooking salt to induce vomiting following ingestion of a nontoxic dose (10 g) of chocolate. Upon admission, the dog was comatose with intermittent seizures and vomiting. Diagnostic tests confirmed salt intoxication (Na: 200 mEq/L, Cl: 180 mEq/L) and metabolic acidosis (pH: 7.18; pCO₂: 39 mmHg; HCO₃: 14.3 mmol/L). Immediate treatment included intravenous fluid therapy, an anticonvulsant, antiemetic, diuretic, low molecular weight heparin, and supplemental oxygen. A fluid therapy protocol was initiated to decrease serum sodium concentration by approximately 2 mEq/L/hr. After 24 hours of intensive care, the patient regained consciousness and volume and acid‐base abnormalities improved. The patient developed a variety of abnormal clinical signs as a result of the severe hypernatremia. After 5 days of treatment, the serum sodium concentration returned to the established reference range. The patient recovered completely in 10 days. New information provided: Severe hypernatremia due to salt ingestion is a rare condition in dogs. All dogs in previous case reports of salt intoxication have died. This case report is the first to report survival of a dog with severe salt intoxication.     

Respiratory failure attributable to moxidectin intoxication in a dog

A 5-month-old 22-kg (48.4-lb) sexually intact male Collie was examined after ingesting a moxidectin-containing deworming medication. The dog was comatose and had respiratory arrest after progressively worsening lethargy, ataxia, and seizures. Exposure was confirmed by isolation of moxidectin from a biopsy specimen of adipose tissue, using liquid chromatography-mass spectroscopy methods. Treatment included use of intermittent positive-pressure ventilation, activated charcoal and cathartic administered enterally, nutrients administered via nasogastric tube, and intensive supportive care. The dog was weaned from a ventilator on day 6 after ingestion and was discharged on day 10. The dog was considered clinically normal during examination 24 days after ingestion. On the basis of the dog reported here and toxicologic data provided by the manufacturer of the deworming product, some Collies may have increased susceptibility to products containing high doses of moxidectin.     

Temporary transvenous cardiac pacing in a dog with diltiazem intoxication

Objective: This case report presents the clinical findings of a dog with diltiazem intoxication and the utilization of temporary transvenous pacing for management of high‐grade second‐degree atrioventricular (AV) block with associated bradycardia and hypotension. Case summary: A nine‐year‐old spayed female Basset Hound, who ingested between 95 and 109 mg/kg of sustained‐release diltiazem exhibited clinical signs of cardiac arrhythmias, bradycardia, hypotension, mental depression and gastrointestinal (GI) upset. Bradycardia was present initially, then was followed by high‐grade second‐degree AV block with ventricular escape. Traditional medications to treat calcium channel blocker (CCB) intoxication, including atropine, calcium gluconate, dopamine and glucagon were initially successful in managing the cardiac rhythm disturbances and hypotension. Twenty‐two hours post‐ingestion, however, the dog became refractory to these medications following sedation for GI decontamination and a temporary transvenous pacemaker was placed. The dog was paced for 19 hours. Transvenous pacing effectively increased heart rate, which increased blood pressure into an acceptable range. The dog was successfully discharged from the hospital following treatment. New or unique information provided: The use of a temporary pacemaker should be considered an acceptable treatment for bradycardia, AV block and hypotension associated with CCB intoxication when conventional medical therapy fails.     

Bilateral hydronephrosis secondary to anticoagulant rodenticide intoxication in a dog

Objective: To describe an unusual site of hemorrhage in a case of anticoagulant rodenticide toxicity. Case summary: A dog treated for Brodifacoum anticoagulant rodenticide intoxication was referred for treatment of thrombocytopenia and dysuria. Sonographic examination revealed a large blood clot within the urinary bladder, extending proximally along both ureters, and a bilateral hydronephrosis. In this dog, management of the vitamin K₁‐dependent coagulopathy was unusually complicated by uremia and thrombocytopenia. New information provided: This is the first reported case of hydronephrosis secondary to anticoagulant rodenticide intoxication in a dog.     

Xylitol intoxication associated with fulminant hepatic failure in a dog

Objective: To describe a case of xylitol intoxication causing fulminant hepatic failure in a dog. Case summary: A 2.5‐year‐old castrated male English Springer Spaniel weighing 26 kg, was presented after ingestion of half of a loaf of bread containing the sweetener xylitol. Toxic effects of the xylitol in this dog included vomiting, mild hypoglycemia and fulminant hepatic failure. Clinical management of acute hepatic failure and subsequent coagulopathy with supportive care and fresh frozen plasma is described. The dog was discharged 3 days after admission after a full clinical recovery. New or unique information provided: This paper describes the clinical consequence and successful treatment of fulminant hepatic failure in a dog following ingestion of xylitol.     

Treatment of accidental ethanol intoxication with hemodialysis in a dog

Objective – To describe the successful treatment of accidental ethanol intoxication with hemodialysis in a dog. Case Summary – A 1.5‐year‐old female intact mixed breed dog was presented in a comatose state believed to be due to ethanol intoxication. The initial 9 hours of supportive care treatment were complicated by multiple seizures and hypothermia, and resulted in only minimal improvement in the dog's level of consciousness. Hemodialysis was implemented and resulted in rapid clinical recovery, corresponding to a rapid decline in serum ethanol concentration. New or Unique Information Provided – To the authors' knowledge, this is the first reported case of using hemodialysis to treat accidental ethanol intoxication in a dog. The patient's initial serum ethanol concentration was higher than those previously reported for cases of accidental ethanol intoxication in dogs, and the serum ethanol concentration was shown to rapidly decline during hemodialysis. Treatment with hemodialysis for severe ethanol intoxication was effective in this case and may be able to decrease morbidity and mortality in some cases.     

Peliosis hepatis and hemoperitoneum in a dog with diphacinone intoxication

Objective: To describe the clinical course of a dog presented with peliosis hepatis and hemoperitoneum in concert with anticoagulant rodenticide intoxication.
Case summary: A 7.75-year-old spayed female Shetland Sheepdog presented with clinical signs consistent with hypovolemia, hemoperitoneum, and a history of bright green stool 3 days before the onset of clinical signs. Initial packed cell volume/total solids were consistent with acute hemorrhage. A coagulation profile showed prolongation in activated clotting time and prolongation of both prothrombin and activated partial thromboplastin time, suggesting abnormal coagulation. Abdominal hemorrhage persisted in the face of normalization of the hemodynamic status and coagulation profile, and treatment with Vitamin K₁. Abdominal ultrasound revealed multiple patchy hypoechoic areas throughout the caudate liver lobe. An exploratory laparotomy was performed 24 hours after presentation and revealed the caudate liver lobe as the source of the hemorrhage. Histopathologic examination of a specimen of the liver was consistent with peliosis hepatis. Toxicologic testing identified diphacinone levels in the blood consistent with anticoagulant rodenticide intoxication. Postoperative recovery was uneventful, and within 48 hours the dog was discharged. The dog returned to full function and a hepatic ultrasound performed 15 months postoperatively showed no significant abnormalities.
New or unique information provided: Exposure to anticoagulant rodenticides may be associated with the development of peliosis hepatis in dogs.     

Coma and respiratory failure due to moxidectin intoxication in a dog

Objective: To describe the clinical consequences following ingestion by a dog of a moxidectin‐containing equine deworming product. Few reports exist concerning the treatment and outcome of severe moxidectin toxicity. Treatment, known factors influencing intoxication, and prognosis are reviewed. Case summary: A 10‐month‐old female Border Collie ingested an unknown quantity of a moxidectin‐containing equine deworming product several hours before presentation. Severe neurological signs subsequently developed and included: ataxia, seizures, coma, and respiratory failure. The dog was treated with supportive care including intravenous fluids, activated charcoal, and positive pressure ventilation. Normal spontaneous respiration returned in 34 hours and the patient was discharged 58 hours after ingestion. Full recovery occurred within 1 week of intoxication. New information provided: This report describes moxidectin intoxication and associated respiratory failure in a dog that required mechanical ventilation. The dog's recovery was rapid. Despite severity of signs, the prognosis for patients with moxidectin intoxication is good with appropriate supportive care.