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.     

Acute polyneuromyopathy with respiratory failure secondary to monensin intoxication in a dog

Objective

To describe a successfully managed case of polyneuropathy and respiratory failure secondary to presumed monensin intoxication.

Case Summary

A 9‐month‐old Australian Shepherd was evaluated for progressive generalized weakness and respiratory distress. Several days preceding presentation, the dog was seen playing with a monensin capsule, and had free access to a barn where the product was stored and where chewed capsules were subsequently found. The dog was presented with flaccid tetraparesis, hyperthermia, and severe respiratory distress. Bloodwork and urinalysis revealed marked increase in serum creatine kinase concentration and presumed myoglobinuria. Cardiac troponin I level was markedly increased. Management included mechanical ventilation for 5 days, fluid‐therapy, active cooling, antimicrobial therapy, analgesia, gastroprotectants, antiemetics, enteral feedings, continuous nursing care, and physiotherapy. Intravenous lipid rescue therapy was administered with lack of improvement in respiratory function and muscle strength. The patient completely recovered and was discharged after 12 days of hospitalization.

New or Unique Information Provided

Monensin intoxication should be considered in the differential diagnosis of acute polyneuromyopathy and respiratory failure in dogs with access to this compound. Respiratory failure secondary to monensin intoxication does not necessarily carry a poor prognosis if mechanical ventilation can be provided as a bridge until return of respiratory function is achieved.     

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.     

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.     

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.     

Aluminium intoxication in a dog

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.     

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.     

Allergic inhalant dermatitis attributable to marijuana exposure in a dog

Exposure to marijuana was believed to be responsible for clinical signs consistent with allergic inhalant dermatitis in a dog. The dog had facial and pedal pruritus associated with bilateral ocular discharge. Clinical signs resolved when the dog was kenneled, but returned when the dog was returned to its home. The results of intradermal skin testing, using a standard tray of 51 inhalant extracts, did not adequately account for the dog's clinical signs. Later, the owners indicated that previous residents of the owners' home had cultivated marijuana intensively inside and outside of the home. Intradermal skin testing with a source of marijuana pollen extract was performed, yielding a positive reaction in the dog and a negative reaction in another dog without clinical or historical evidence of allergic inhalant dermatitis. The affected dog was treated successfully and exclusively by hyposensitization with marijuana pollen extract.     

Metastatic calcification in a dog attributable to ingestion of a tacalcitol ointment

A 22-week-old 21-kg female Bernese Mountain Dog ingested a topical antipsoriatic preparation containing the synthetic vitamin D analog tacalcitol. The dog died after a history of lethargy, recumbency, paresis of the hindlimbs, increased rectal temperature, dyspnea, and hematemesis. Histologic examination revealed metastatic calcification in the kidneys, lungs, myocardium, brain, stomach, and tear glands. The appearance of soft tissue mineralization in multiple organs is consistent with hypercalcemia derived from excessive vitamin D uptake. Oral toxicity studies for tacalcitol in the dog are not available, but the present report emphasizes the extraordinary toxic risk of drugs containing this vitamin D analog to dogs.     

Recurring tetraparesis attributable to a heartworm in the epidural space of a dog

Recurring nonambulatory tetraparesis caused by a heartworm in the epidural space was diagnosed in a dog. On myelography and digital subtraction imaging, the parasite appeared as a large extradural mass. Surgical removal of a mature, female Dirofilaria immitis resulted in resolution of the neurologic signs.     

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.     

The use of sarmazenil in the treatment of a moxidectin intoxication in a foal

A13-day-old Arabian Thoroughbred filly weighing 40 kg (88 1b) was presented to the University of Zurich Equine Clinic with a history of depression after deworming with moxidectin at a dose of 2 mg/kg (recommended dose 0.4 mg/kg body weight)^a the day before admission. The foal was found recumbent 12 hours after drug administration and was in an unconscious state 6 hours later     

Respiratory paralysis secondary to epidural anesthesia in a dog

Transient respiratory paralysis developed in a 12-year-old spayed female Cocker Spaniel that received an anesthetic epidurally for excisional biopsy of perianal masses. Paralysis developed almost immediately after injection of 2.5 ml of 2% lidocaine (1 ml/4.9 kg), and was managed by mechanical ventilation and appropriate fluid therapy IV until spontaneous respiration returned. The respiratory paralysis was attributed to the excessive cranial extent of the anesthetic block.