Use of pamidronate to reverse vitamin D3-induced toxicosis in dogs.

OBJECTIVES: To determine whether pamidronate disodium can reduce vitamin D3-induced hypercalcemia in dogs and whether combination treatment with calcitonin is more effective than treatment with pamidronate alone. ANIMALS: 20 clinically normal male Beagles. PROCEDURE: All dogs were given 8 mg of cholecalciferol (CCF)/kg of body weight once orally, then were assigned randomly to 4 groups of 5 dogs each. Dogs were given 0.9% NaCl solution IV (group 1), calcitonin SC and 0.9% NaCl solution IV (group 2), pamidronate and 0.9% NaCl solution IV (group 3), or a combination of all 3 agents (group 4). Dogs were observed for 28 days, and serial blood and urine samples were collected for determination of serum biochemical, electrolyte, and 25(OH)D3 values, CBC, and urine mineral excretion. Samples of kidney, stomach, lung, aorta, liver, duodenum, and brain were evaluated by light microscopy and quantitative mineral analysis. RESULTS: Two dogs in group 1 were euthanatized 4 days after CCF administration because of severe clinical signs of disease. Dogs in group 3 lost less weight and had significantly lower serum phosphorus, total and ionized calcium, and urinary zinc concentrations, compared with dogs in group 1. On day 4, serum urea nitrogen concentration was significantly lower in dogs of groups 3 and 4, compared with dogs in group 1. Mild to moderate mineralization of kidneys and stomach were observed in the 2 group-1 dogs euthanatized on day 4. CONCLUSIONS: Pamidronate administration effectively prevents CCF-induced hypercalcemia and mineralization of soft tissues. CLINICAL RELEVANCE: Pamidronate is a potentially useful antidote against CCF toxicosis in dogs.     

Use of cyclosporine to treat granulomatous meningoencephalitis in three dogs

Use of cyclosporine to treat granulomatous meningoencephalitis in three dogs Three dogs with a presumptive diagnosis of granulomatous meningoencephalitis were treated with orally administered cyclosporine. In 2 dogs, cyclosporine administration replaced initial corticosteroid administration, and in 1 dog, cyclosporine was the only treatment used. One dog had the focal form of the disease in the brainstem, 1 dog had the focal form in the forebrain associated with a concurrent ocular form, and 1 dog had the disseminated form of disease. At 12-month follow-up, the 2 dogs with the focal form of the disease had no clinical signs. The dog with the disseminated form improved only partially, and euthanasia was performed 3 weeks after initial evaluation. Cyclosporine was considered effective at an initial dosage of 6 mg/kg (2.7 mg/lb) every 12 hours. Adverse effects associated with cyclosporine administration included transient lymphopenia, excessive shedding, and focal symmetric hair discoloration.     

Use of cabergoline to treat primary and secondary anestrus in dogs

OBJECTIVE: To determine whether cabergoline would be safe and effective for induction of estrus in dogs with primary or secondary anestrus. DESIGN: Prospective case series. ANIMALS: 6 privately owned otherwise healthy pure-bred dogs with primary or secondary anestrus. PROCEDURE: Dogs were treated with cabergoline (5 microg/kg [2.3 microg/lb], p.o., q 24 h) until 2 days after the onset of proestrus. Follicular development was assessed by means of cytologic examination of vaginal smears; ovulation was assessed by measuring serum progesterone concentration 3 weeks after the onset of estrus. Five bitches were mated during behavioral estrus. RESULTS: All dogs had normal estrus periods, and all 5 dogs that were mated whelped normal litters. Mean duration of cabergoline treatment was 16 days. None of the dogs had any adverse effects associated with cabergoline administration. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that administration of cabergoline is safe and effective for treatment for primary and secondary anestrus in dogs.     

Inherited copper toxicosis in the Bedlington terrier: the prevalence in asymptomatic dogs

Copper toxicosis in the Bedlington terrier is an inherited defect. This paper describes the investigation of 62 Bedlington terriers, none of which had shown any clinical signs of liver disease, in order to assess the prevalence of copper toxicosis in the breed in the United Kingdom. Twenty one (33·9 per cent) of the dogs investigated had abnormally high levels of copper in the liver. No reliable circulating haematological or biochemical parameters were found to identify those dogs with increased hepatic copper levels and the diagnosis could only be established by liver biopsy. Affected dogs had liver copper levels of between 257·5 and 2558·0 μpg per g of wet weight (1163·8 ± 164 μg/g, mean ± SEM) compared with normal dogs which had between 9·9 and 118·6 μg/g of wet weight (49·0 & 4·4 μg/g, mean ± SEM). Copper accumulation in the liver of affected dogs could also be detected on histological examination using special stains.     

Use of inhaled medications to treat respiratory diseases in dogs and cats

Noninfectious disorders of the respiratory tract, including laryngitis, tracheitis, bronchitis, and asthma are common problems in dogs and cats. Traditional therapies have often included corticosteroids and bronchodilators given by mouth or injection. Side effects of this form of treatment can be severe and can result in cessation of therapy. Inhaled corticosteroid drugs are not as absorbed into the systemic circulation, do not result in significant side effects, and are now the standard of care for dogs and cats with respiratory diseases that would otherwise be treated with systemic medications.     

Acute copper toxicosis in the Canada goose.

Acute copper toxicosis resulted in Canada geese, Branta canadensis, following ingestion of copper sulfate at about 600mg/kg from a small man-made pond on a game farm. The lesions were those associated with copper toxicosis in other avian species. The primary pathologic change was necrosis and sloughing of the proventriculus and gizzard. A greenish discoloration of the lungs also occurred.     

Bread dough toxicosis in dogs

Objective: To provide information on the ingestion, and subsequent toxicity, of raw bread dough in dogs. Case summary: A report from the ASPCA animal poison control center (APCC) files of 3 cases of ingestion of raw bread dough by dogs. Clinical signs included vomiting, ataxia, blindness, hypothermia, and recumbency. All dogs were successfully treated for ethanol toxicosis. New information: Ingestion of bread dough can cause gastric obstruction, bloat, or ethanol toxicosis. The treatment of ethanol toxicosis, including decontamination, IV fluids, management of metabolic acidosis, and hypoglycemia is discussed. Yohimbine can be used in cases where the dog is comatose or has developed severe respiratory depression.     

Dinoseb toxicosis in two dogs

Two male English Setters were noticed to be breathing rapidly, hyperexcitable, and atactic after roaming a rural area for 2 hours. Both dogs' cost were stained with yellow liquid. One dog died while en route to the veterinarian. Treatment was begun for the surviving dog for what was initially diagnosed to be organophosphorus or carbamate insecticide toxicosis. Before the diagnosis could be confirmed, the second dog died. The yellow liquid on the dogs' skin was identified as dinoseb in high concentrations. Dinoseb is an acutely toxic, substituted dinitrophenolic herbicide believed to act as an uncoupler of electron transport from oxidative phosphorylation.     

Use of intravenous lidocaine to treat dexmedetomidine-induced bradycardia in sedated and anesthetized dogs

ObjectiveTo assess cardiopulmonary function in sedated and anesthetized dogs administered intravenous (IV) dexmedetomidine and subsequently administered IV lidocaine to treat dexmedetomidine-induced bradycardia.Study designProspective, randomized, crossover experimental trial.AnimalsA total of six purpose-bred female Beagle dogs, weighing 9.1 ± 0.6 kg (mean ± standard deviation).MethodsDogs were randomly assigned to one of three treatments: dexmedetomidine (10 μg kg^–1 IV) administered to conscious (treatments SED1 and SED2) or isoflurane-anesthetized dogs (end-tidal isoflurane concentration 1.19 ± 0.04%; treatment ISO). After 30 minutes, a lidocaine bolus (2 mg kg^–1) IV was administered in treatments SED1 and ISO, followed 20 minutes later by a second bolus (2 mg kg^–1) and a 30 minute lidocaine constant rate infusion (L-CRI) at 50 (SED1) or 100 μg kg^–1 minute^–1 (ISO). In SED2, lidocaine bolus and L-CRI (50 μg kg^–1 minute^–1) were administered 5 minutes after dexmedetomidine. Cardiopulmonary measurements were obtained after dexmedetomidine, after lidocaine bolus, during L-CRI and 30 minutes after discontinuing L-CRI. A mixed linear model was used for comparisons within treatments (p < 0.05).ResultsWhen administered after a bolus of dexmedetomidine, lidocaine bolus and L-CRI significantly increased heart rate and cardiac index, decreased mean blood pressure, systemic vascular resistance index and oxygen extraction ratio, and did not affect stroke volume index in all treatments.Conclusion and clinical relevanceLidocaine was an effective treatment for dexmedetomidine-induced bradycardia in healthy research dogs.     

Hypercalcemia secondary to cholecalciferol rodenticide toxicosis in two dogs

Hypercalcemia secondary to cholecalciferol rodenticide toxicosis was identified in two dogs. The first dog died shortly after admission. The second dog responded to treatment with sodium chloride solution, prednisolone, furosemide, and calcitonin. Treatment was needed for a longer period than anticipated and the serum calcium concentration did not stabilize for approximately one month. Although not conclusively demonstrated, calcitonin was considered the cause of severe anorexia. This new class of rodenticides has great toxic potential for dogs, and it is recommended that serum calcium concentration be carefully monitored as treatment for hypercalcemia is gradually withdrawn.     

Sodium fluoride/copper naphthenate toxicosis in cattle.

Fourteen cattle on a Kansas pasture died from ingestion of a wood preservative compound containing sodium fluoride and copper naphthenate. Clinical signs included depression, anorexia, ataxia, diarrhea, and recumbency. Grossly visible lesions included perirenal edema, pale kidneys, and forestomach ulceration. All 3 cows that had postmortem evaluations had extensive renal cortical tubular necrosis. Tissue concentrations of fluoride were slightly elevated above expected background levels, while copper tissue concentrations were not elevated. The findings indicated that the sodium fluoride caused renal tubular necrosis leading to renal failure. Copper naphthenate may have contributed to abomasal ulceration; however, tissue copper concentrations indicated that copper from the formulation was not appreciably absorbed from the gastrointestinal tract.     

Investigations of therapeutic measures for disophenol toxicosis in dogs.

Acute disophenol toxicosis, induced in 10 dogs by giving 33, 35, or 40 mg of disophenol/kg of body weight, was treated with the antipyretic dipyrone, lactated Ringer's infusions, or ice baths. Rectal temperature and estimates of hemoglobin concentration, packed cell volume, and total white blood cell count and differential count were recorded. Higher hemogram values were sometimes observed for dogs dying of the toxicosis. Toxicosis was induced in 5 other dogs which were not treated; 1 of these, given the low dose of disophenol, recovered. Two of 3 dogs (67%) treated with the antipyretic recovered, 0 of 2 (0%) given lactated Ringer's infusion recovered, and 2 of 5 dogs (40%) treated with ice baths recovered. One of the surviving dogs treated with antipyretic was given the low disophenol dose and all the other survivors were given the medium disophenol dosage level.