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.     

Clinical and histologic outcome in a dog surviving massive hepatic necrosis

This report describes the clinical and histologic recovery of a 2‐year‐old mixed‐breed dog presented with hypovolemic shock, markedly increased serum alanine amino transferase activity, and hemoabdomen. Emergency exploratory surgery revealed a friable liver with multiple capsule hemorrhages necessitating removal of the left lateral lobe. Histologic evaluation showed acute massive hepatic necrosis with centrilobular and midzonal distribution. The dog survived, and all monitored laboratory values normalized within 7 weeks. A liver biopsy taken 8 weeks after presentation revealed normal hepatic architecture with a few, randomly distributed neutrophilic foci. Follow‐up included intermittent determination of liver variables including liver function tests for a period of 7 years. The dog's health status, and all test results remained normal during this time. Complete recovery and good long‐term quality of life after life‐threatening acute liver failure secondary to massive hepatic necrosis is possible in dogs.     

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.     

Acute tracheal obstruction associated with anticoagulant rodenticide intoxication in a dog

An adult female neutered crossbred dog was referred in respiratory distress. Thoracic radiographs revealed tracheal narrowing with a soft tissue opacity dorsal to the trachea, near the thoracic inlet, and a patchy interstitial pulmonary infiltrate. The tracheal narrowing was thought to be due to a combination of intraluminal haemorrhage and mediastinal haemorrhage resulting from a coagulopathy caused by anticoagulant rodenticide intoxication. Treatment included supportive care and administration of vitamin K1, and the dog showed a complete resolution of the clinical signs.     

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.     

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.     

Renal failure associated with pericardial effusion in a dog.

Signs of heart failure due to cardiac tamponade developed in a young dog with previously unrecognized renal disease. The uremic syndrome was considered the likely cause of the effusive pericarditis found at necropsy. In a review of necropsy records from 150 dogs with renal disease, 11 had pericardial lesions.     

Treatment of a dog with severe baclofen intoxication using hemodialysis and mechanical ventilation

Objective: This case report describes the successful management of a dog with coma and respiratory depression due to severe baclofen intoxication. Case summary: A Doberman Pinscher mixed breed dog ingested 500 mg (20 mg/kg) of baclofen. Signs of severe intoxication included coma and profound respiratory muscle weakness. The dog was supported with positive pressure ventilation and treated with one session of hemodialysis. Weaning from the ventilator was achieved within 4 hours of hemodialysis, and recovery from coma occurred over the following 12–36 hours. The dog regained full neurologic function and was normal at discharge following 3 days of hospitalization. New or unique information provide: Severe central nervous system depression and respiratory depression due to baclofen intoxication can be life threatening. In addition to other supportive care, hemodialysis may hasten recovery and ventilatory support may be essential to achieve a positive outcome. With successful treatment, toxicity can be decreased and the associated life‐threatening central nervous system and ventilatory depression can resolve. Prognosis for return of normal function is excellent.     

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.     

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

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.     

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.     

Chronic liver disease associated with high hepatic copper concentration in a dog

An 8-month-old dog admitted for routine castration was found to have ascites. Liver biopsy revealed inflammation, fibrosis, and a copper concentration of 1,300 ppm on a dry weight basis. As cirrhosis developed, the copper concentration decreased without chelator treatment. At necropsy, the dog had cirrhosis, but the hepatic copper concentration was only 730 ppm.     

Transient leucopenia, thrombocytopenia and anaemia associated with severe acute phenobarbital intoxication in a dog

A nine-year-old Labrador retriever dog was admitted to the emergency unit of the Hebrew University Veterinary Teaching Hospital with acute-onset tremors and coma. It had recently ingested a large quantity of phenobarbital and had a high serum phenobarbital concentration. On this basis, a diagnosis of acute phenobarbital intoxication was made. Significant leucopenia, thrombocytopenia and mild anaemia developed on the third day after admission. The leucopenia resolved on day 6 and the thrombocytopenia on day 13. The red blood cell count remained low for the next month. The dog was discharged on day 13 at which time it was ambulatory but weak. It was completely recovered clinically eight days later. In summary, high levels of serum phenobarbital as a result of acute intoxication induced pancytopenia, which improved when the serum phenobarbital level was normalised.