Presumptive hepatotoxicity and rhabdomyolysis secondary to phenazopyridine toxicity in a dog

Objective – To describe a rare, but potential clinical manifestation of phenazopyridine (PAP) toxicity in a dog. Case Summary – A 6‐year‐old spayed female Chihuahua was evaluated for ataxia and dysphagia after ingestion of 200 mg (66 mg/kg) of PAP hydrochloride. The dog was presented to the hospital with shifting leg lameness involving all 4 limbs, which progressed to reluctance to walk and severe diffuse muscle hyperesthesia. Clinical laboratory abnormalities included marked increases in serum alanine aminotransferase, aspartate aminotransferase, creatine kinase, mild increases in alkaline phosphatase, and increased c‐Tnl‐troponin concentration. Treatment included administration of intravenous fluids, muscle relaxants, pain medications, and hepatoprotectants for 5 days in the hospital, and medical management at home for an additional 5 days. Follow‐up examinations performed 1 and 6 months after initial presentation revealed the dog to be clinically healthy with serum biochemical profiles within reference intervals. New or Unique Information Provided – The purpose of this report is to describe an unusual manifestation of PAP toxicosis in a dog, which has not been previously reported in the literature. A review of the ASPCA Animal Poison Control Center database revealed 347 cases of PAP exposure in dogs during 2000–2009 underscoring the importance of being aware of this toxicity in the dog.     

Negative hepatic computed tomographic attenuation pattern in a dog with vacuolar hepatopathy and hepatic fat accumulation secondary to cushing's syndrome

This report describes an unusual computed tomographic (CT) hepatic pattern, characterized by negative attenuation values (from –19.59 to –28.85 Hounsfield Units, HU) in a canine patient with severe Cushing's syndrome. Attenuation values of the splenic parenchyma (63.26 HU) and abdominal fat (–118.34 HU) were within normal limits. The negative hepatic attenuation values allowed a CT diagnosis of severe hepatic fatty infiltration that was subsequently confirmed by tissue‐core biopsy and histopathological examination.     

Pharmacokinetics,pharmacodynamics and clinical use of trazodone and its active metabolite m‐chlorophenylpiperazine in the horse

Trazodone is a serotonin receptor antagonist and reuptake inhibitor used extensively as an anxiolytic in human and small animal veterinary medicine. The aims of this study were to determine the pharmacokinetics of oral trazodone in experimental horses and to evaluate the effect of oral trazodone in clinical horses. Six experimental horses were administered trazodone at 7.5 or 10 mg/kg. Plasma concentrations of trazodone and its metabolite (m‐CPP) were determined via UPLC‐MS/MS. Noncompartmental pharmacokinetic analysis, sedation and ataxia scores were determined. Trazodone was rapidly absorbed after oral administration with a maximum concentration of 2.5–4.1 μg/ml and half‐life of the terminal phase of approximately 7 hr. The metabolite was present at low levels in all horses, representing only 2.5% of the total area under the curve. In experimental horses, concentration‐dependent sedation and ataxia were noted, lasting up to 12 hr. For clinical cases, medical records of horses treated with trazodone for various abnormal behaviours were reviewed and data were summarized. Trazodone was successful in modifying behavioural problems to some degree in 17 of 18 clinical cases. Tolerance and subsequent lack of drug effect occurred in two of 18 clinical cases following 14 or 21 days of use. In both populations of horses, adverse effects attributed to trazodone include oversedation, muscle fasciculations and transient arrhythmias.     

Suspected congenital hyperinsulinism in a Shiba Inu dog

A 3-month-old male intact Shiba Inu dog was evaluated for a seizure disorder initially deemed idiopathic in origin. Seizure frequency remained unchanged despite therapeutic serum phenobarbital concentration and use of levetiracetam. The dog was documented to be markedly hypoglycemic during a seizure episode on reevaluation at 6 months of age. Serum insulin concentrations during hypoglycemia were 41 U/μL (reference range, 10-29 U/μL). The dog was transitioned to 4 times per day feeding, diazoxide was started at 3.5 mg/kg PO q8h, and antiepileptic drugs were discontinued. No clinically relevant abnormalities were identified on bicavitary arterial and venous phase contrast computed tomographic imaging. The dog remained seizure-free and clinically normal at 3 years of age while receiving 5.5 mg/kg diazoxide PO q12h and twice daily feeding. Seizures later occurred approximately twice per year and after exertion, with or without vomiting of a diazoxide dose. Blood glucose curves and interstitial glucose monitoring were used to titrate diazoxide dose and dosing interval. Congenital hyperinsulinism is well recognized in people but has not been reported in veterinary medicine.     

Symblepharon secondary to ophthalmomyiasis externa in a dog

A 4-month-old crossbred female dog presented with complaints of poor vision and odd appearance of the eyes. At the age of a month, the animal was found lying in a railway road in a very bad condition and was rescued from death. At that time, the patient was presented with severe bilateral ocular discharge, and from both eyes, dipterous fly larvae were extracted. The dog was given symptomatic treatment (deworming, topical and systemic antibiotics, nutritional support) but never regained a normal eye appearance. At the time of the initial presentation, it had severe vision impairment because of bilateral cicatricial symblepharon, total in the left eye and occupying 3/4 of the cornea in the right eye. Surgery was proposed to attempt a resolution. Superficial keratectomy was performed in both eyes. After a midline incision in the cornea, the conjunctiva was dissected away. The conjunctiva was apposed to and sutured to the limbus and secured in the upper and lower conjunctival fornix. Additionally, in the left eye, a lateral canthotomy and canthoplasty were performed to enlarge the size of the eyelid opening. The corneal epithelium healed without complications, the patient regained vision, and after 36 months of follow-up, no recurrences were observed. To the authors' knowledge, this is the first report of symblepharon secondary to ophthalmomyiasis externa in a dog.     

Pneumothorax secondary to pulmonary thromboembolism in a dog

Objective – To describe a case of spontaneous pneumothorax secondary to pulmonary thromboembolism possibly associated with pituitary dependent hyperadrenocorticism.
Case Summary – A 7-year-old spayed female Collie weighing 26 kg was referred for evaluation of spontaneous pneumothorax. An exploratory thoracotomy was performed and revealed 2 lung lobes to be diffusely hemorrhagic and they were resected. Histologic examination of multiple sections documented diffuse thromboembolism. A 2–3 cm thrombus was visualized distal to the bifurcation of the pulmonary artery during an echocardiographic examination postoperatively. The dog was discharged to the owner after recovery from surgery. The thrombus had resolved at the 4-week recheck examination. Diagnosis of pituitary dependent hyperadrenocorticism was confirmed based on follow-up endocrine testing.
New or Unique Information Provided – This is the first report of pulmonary thromboembolism causing spontaneous pneumothorax in the dog.     

Priapism secondary to penile metastasis in a dog

A 4-year-old, male Newfoundland cross was presented for lethargy, anorexia, and dysuria. The main clinical finding was an enlarged and painful prostate gland. While the dog was hospitalized, priapism developed. Following euthanasia, microscopic examination revealed that a carcinoma involving both bladder and prostate gland had widely metastasized to the penile vasculature.     

Suspected spontaneous hyperadrenocorticism in a young experimental beagle dog

A 6-month-old female beagle dog, assigned to the low-dose group in a toxicity study, was evaluated for compound toxicity, and spontaneous hyperadrenocorticism was suspected. The animal had an externally apparent distended abdomen on clinical examination upon arrival. Pre-dose clinical pathology showed slightly higher erythroid parameters and stress leukogram on hematology; plasma biochemistry showed higher total protein, gamma-glutamyl transferase, total cholesterol, and triglyceride levels than the reference data. On necropsy, a prominent increase in adipose tissues of the subcutis and abdomen and increased weight of the adrenal gland and liver were observed. Histopathology revealed diffuse hyperplasia of adrenocortical cells in the zona fasciculata and reticularis, cortical atrophy of the thymus, and abundant glycogen accumulation in the hepatocytes. These findings were incidental and not test-substance-related. Electron microscopy of the adrenocortical cells in the zona fasciculata revealed decreased typical translucent lipid droplets, increased electron-dense lipid droplets, and abundant smooth endoplasmic reticulum and lysosomes. Additionally, increased numbers of various sizes and forms of mitochondria with tubular, vesicular, or lamellar cristae compared to that of normal animals were observed. These ultrastructural characteristics of the adrenocortical cells suggested hyperfunction. The pre-dose plasma cortisol levels were slightly higher than those of other females assigned to the toxicity study, while plasma adrenocorticotropic hormone levels were within the normal range. These findings indicate that hyperadrenocorticism is a possible cause of the systemic changes in this case.     

Gastric granulomatous cryptococcosis mimicking gastric carcinoma in a dog

Summary

An ulcerated lesion resembling a tumour in the lesser curvature of the stomach of a 3‐year‐old male Dobermann pinscher was found to be caused by Cryptococcus neoformans. The dog had been vomiting for two months and had slight leucocytosis and anaemia. Biopsies of the ulcerated lesion revealed granulomatous inflammation and many cryptococci, which were particularly prominent in PAS and mucicarmine stained sections. No other lesions were found at necropsy.     

Suspected uveal metastasis of a nail bed melanoma in a dog

A 13-year-old Golden Retriever was referred for evaluation of generalized corneal edema, dyscoria, and suspected glaucoma affecting the right eye. The dog exhibited no signs of systemic illness, but had a history of a melanoma of the nail bed of the first digit of the right hind limb, excised 1 year previously. Ophthalmologic examination revealed diffuse corneal edema, mild anterior uveitis, glaucoma and a mass within the right iris. Enucleation was performed and histopathologic evaluation of the globe revealed the iris to be infiltrated with an anaplastic melanoma, suspected to represent a metastasis of the original nail bed tumor.     

Cervical syringohydromyelia secondary to a brainstem tumor in a dog

An 11-year-old male Pekingese was evaluated because of a history of head tilt. Neurologic examination revealed a right-sided head tilt, ataxia, scoliosis, and proprioceptive deficits. Diagnostic testing included magnetic resonance imaging (MRI) of the head and neck. After IV administration of gadopentetate dimeglumine, an extra-axial, highly contrast-enhanced mass in the brainstem, cerebellar herniation, and syringohydromyelia were detected via MRI. The dog was treated with corticosteroids and radiation therapy of the mass for 4 weeks (total dose, 42.5 Gy). Magnetic resonance imaging was repeated 9 weeks and 6 months after radiation therapy; compared with the initial findings, a reduction in the size of the brainstem mass was observed in both MRI scans. The third MRI scan also revealed a normal cerebellar shape, no evidence of herniation, and resolution of syringohydromyelia in the dog at that time. It is recommended that whenever syringohydromyelia is observed via MRI, a primary cause (cranial or caudal to the affected region) should be sought.