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.     

Thallium toxicosis in a Pit Bull Terrier.

Thallotoxicosis is described in an adult Pit Bull Terrier. The dog exhibited anorexia, emesis, weakness, conscious proprioceptive deficits, and a hemorrhagic diarrhea before death. A severe, acute necrotizing enterocolitis was evident upon histological examination, as was a multifocal to coalescing pulmonary edema. Liver and kidney thallium concentrations were 18 and 26 ppm, respectively. The source of the thallium was determined to be thallium sulfate obtained by a person with the intent to harm family members. Although thallium has not been produced in the United States for 20 years, this report demonstrates the need to consider thallium toxicosis as a differential diagnosis for animals presenting with vague and mixed gastrointestinal and neurological signs.     

Diagnosis and treatment of thallium toxicosis in a dog

A case of chronic thallium toxicosis in a dog is described. The difficulties in diagnosis in the absence of a history of known ingestion of the agent are discussed and a method of increasing urinary thallium to detectable levels is described.     

Severe reaction to intravenous administration of an ionic iodinated contrast agent in two anesthetized dogs

CASE DESCRIPTION: Acute severe systemic reactions developed during i.v. administration of an ionic iodinated contrast agent (iothalamate meglumine) in 2 dogs undergoing contrast-enhanced computed tomography. CLINICAL FINDINGS: Both dogs developed marked changes in heart rate and systolic arterial blood pressure during or immediately after i.v. administration of the contrast agent. The first dog became profoundly hypertensive and bradycardic with poor oxygenation, apparent bronchospasm, and prolonged diarrhea. The second dog became hypotensive and tachycardic with erythema on the ventral aspect of the abdomen and pelvic limbs, periocular edema, and diarrhea. TREATMENT AND OUTCOME: Both dogs were treated for shock by means of i.v. fluid administration, and anesthesia was discontinued. The first dog was placed on a ventilator to improve oxygenation but was hypertensive and unresponsive for 6.5 hours following contrast agent administration. Bloody diarrhea persisted once consciousness was regained. The dog was discharged 3 days after contrast agent administration, and diarrhea resolved 15 days later. The second dog responded to phenylephrine administration, but urine output appeared low immediately following recovery from anesthesia. Urine output was normal the following day, and the dog was released 36 hours after contrast administration with no residual adverse effects. CLINICAL RELEVANCE: Findings highlighted the potential risk for severe reactions associated with i.v. administration of ionic iodinated contrast agents in dogs. Both hypertensive and hypotensive responses were seen. Supportive care for systemic manifestations was effective in these 2 dogs, and extended hospitalization was not necessary.     

The effect of Prussian blue and sodium-ethylenediaminetetraacetic acid on the faecal and urinary elimination of thallium by the dog.

After oral administration of sublethal doses of thallium (lower than 10 mg/kg) to dogs, 75.5 +/- 3.9 per cent of the dose was eliminated from the body--47 per cent faecal and 28 per cent urinary. Cumulative excretion reached 50 and 70 per cent after 10 and 25 days respectively, and was almost complete after 75 days. This was slightly lower at higher doses. The total body-burden of thallium, calculated from the cumulative excretion, decreased exponentially for at least the first 40 days with a half-time (T 1/2) of 6.5 days. Oral doses of Prussian blue after 10 days resulted in an acceleration of the thallium elimination from the body (T 1/2 2.5 days), an increase of the faecal (49 per cent) and a decrease of the urinary excretion (18 per cent). Nevertheless, the cumulative faecal and urinary thallium excretion was not influenced. Minor transitory influences of Prussian blue on the faecal thallium excretion could be observed up to day 26. After 40 days, Prussian blue could no longer influence the faecal thallium excretion. At no time did sodium-ethylenediaminetetraacetic (Na2EDTA) acid significantly change faecal or urinary thallium excretion.     

Pharmacokinetics and preliminary observations of behavioral changes following administration of midazolam to dogs

The pharmacokinetics of midazolam were investigated following intravenous and intramuscular administration of 0.5 mg of midazolam hydrochloride/kg of body weight to five healthy mixed-breed dogs. One dog also received the same dose of midazolam by oral and rectal routes. The disposition of midazolam following intravenous administration was characterized by very rapid and relatively extensive distribution followed by rapid elimination. Mean (+/- SD) apparent volume of distribution was 3.0 +/- 0.9 l/kg, mean elimination half-life was 77 +/- 18 min, and clearance was 27 +/- 3 ml/kg/min. Following intramuscular administration, absorption was rapid and complete. A mean peak midazolam concentration of 549 +/- 121 ng/ml was reached within 15 min, and systemic availability was over 90% in each dog. Oral administration to one dog resulted in peak midazolam concentrations within 10 min and a systemic availability of 69%. Rectal administration to the same dog yielded very low systemic availability. Midazolam was extensively bound to canine plasma proteins, with the unbound fraction representing less than 4% of the total plasma midazolam concentration. Plasma samples were also assayed for the presence of the major metabolites, 1-OH and 4-OH midazolam. Neither metabolite were detected, probably as a result of rapid elimination of these compounds by hepatic glucuronidation. Behavioral responses to administration of midazolam included initial signs of profound weakness, ataxia and transient agitation followed by a period of quiesence. A normal behavior pattern returned within 2 h of midazolam administration.     

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.     

ASYSTOLE ASSOCIATED WITH IOHEXOL MYELOGRAPHY IN A DOG

This is areport of a 10-year-old female neutered Doberman Pinscher with a clinical diagnosis of myelopathy. The dog was anesthetized using oxymorphone, thiopental, and halothane in oxygen for a cerebrospinal tap and a myelogram. Iohexsal injection into the subarachnoid space by lumbar puncture was uneventful. Additional iohexal was given into the cerebellomjedullary cistern. Immediately following iohexal administration into the cerebellomedullary cistern, several electrocardiographic changes occurred. Two extended periods of asystole responded to intravenous glycopyrrolate administration. A slow multiform ventricular escape rhythm was established after the second dose of glycopyrrolate. Ultimately, atrial activity with apparent A V dissociation resumed, atrial fibrillation developed, and the rhythm converted to normal sinus rhythm. The dog had a normal cardiac examination the following day. Two days later, the dog was anesthetized using a similar anesthetic regimen with maintance on isoflurane in oxygen for a hemilaminectomy. The dog recovered uneventfully from surgery and was discharged 2 days later.     

Hemoperitoneum secondary to traumatic rupture of an adrenal tumor in a dog

Hemoperitoneum secondary to traumatic rupture of an adrenocortical adenocarcinoma was diagnosed in a 10-year-old male dog. Immediate surgical attention was required to remove the tumor and to control hemorrhage. The dog appeared to develop transient hypoadrenocorticism after surgery, but recovered with short-term exogenous corticosteroid administration. At 6 months after surgery, the dog was clinically normal.     

Suspected anaphylactoid reaction following intravenous administration of a gadolinium‐based contrast agent in three dogs undergoing magnetic resonance imaging

ObservationsAnaphylactoid reactions were suspected in three dogs following the intravenous administration of the contrast agent gadobenate dimeglumine 0.05 mmol kg^?1 (Multihance^®).Case 1: A 14 kg 6–year–old atopic female dog was anaesthetized for brain magnetic resonance imaging (MRI). All monitored parameters remained stable during the procedure. Fifteen minutes following MR completion; facial, peri–orbital and sublingual oedema were noted. Resolution of the oedema was rapid and uneventful following treatment of clinical signs over 2 hours.Case 2: A 16 kg 10–month–old male dog was anaesthetized for brain and neck MRI. Ten minutes after MR contrast intravenous (IV) injection; heart rate (HR) increased (85–120 beats minute^?1), mean arterial blood pressure (MAP) decreased (from 70 to 43 mmHg) and Pe′CO₂ decreased (from 4.66 to 3.19 kPa). Labial, periorbital and lingual oedema were noted. Clinical signs responded to fluid bolus administration. The dog vomited in recovery but oedema resolved within one hour.Case 3: A 34 kg 2–year–old atopic male dog was anaesthetized for head MRI. Within 5 minutes of MR contrast IV injection; the dog suffered severe cardiovascular collapse. MRI procedure was aborted and administration of anaesthetics discontinued. Aggressive IV fluid resuscitation and IV epinephrine administration were necessary to re–establish cardiovascular stability. Some periorbital and labial oedema were noted. The dog vomited once and had soft faeces but made a complete recovery.ConclusionsThe administration of contrast medium may result in mild to severe anaphylactoid reactions.     

Verapamil administration for acute termination of supraventricular tachycardia in dogs

Verapamil, a calcium channel-blocking drug, was administered IV at a dosage that ranged from 0.05 to 0.15 mg/kg of body weight to 14 dogs with supraventricular tachycardia. The dosage was titrated, administering 0.05 mg/kg every 5 to 30 minutes following the initial 0.05 mg/kg dose in all but 1 dog. The drug terminated the arrhythmia in 12 dogs and slowed the ventricular rate in 1 dog. One dog was unresponsive to verapamil administration and became transiently hypotensive after the administration of a total dose of 0.15 mg/kg over 5 to 6 minutes. Various arrhythmias occurred after verapamil administration, but none required additional treatment or caused serious sequelae. Verapamil was an effective treatment for acutely converting supraventricular tachycardia to sinus rhythm in these dogs. It appears to be safe when administered in the aforementioned dosage range.     

Proliferative glomerulonephritis and chronic active hepatitis with cirrhosis associated with Corynebacterium parvum immunotherapy in a dog

Ivermectin, a broad-spectrum antiparasitic agent, was believed responsible for signs of CNS dysfunction in a dog. Within 2 hours of oral administration of ivermectin, the dog had hind limb ataxia. Neurologic signs progressed rapidly until the dog was in a semicomatose state at admission 20 hours later. The dog improved gradually under supportive care. The ivermectin had been given for suspected endoparasitism. Clinical signs were similar to those reported in dogs with clinical and experimental exposure to ivermectin.     

Adipsic hypernatremia in a dog with antithyroid antibodies in cerebrospinal fluid and serum

A 4-year-old, male Labrador retriever, weighing 27 kg, presented with abrupt clinical signs including mental retardation, circling and head pressing. The dog never ingested water by choice. An adipsia of the dog was persisted and developed to hypernatremia with artifactual hyperchloremia. Serial endocrine results and image findings were suggestive of a hypothyroidism. The dog revealed the presence of antithyroid antibodies in the cerebrospinal fluid and serum. With the administration of levothyroxine sodium, his neurologic signs were alleviated within the first week of treatment and adipsia was also resolved.     

Ketoconazole therapy in a dog with systemic cryptococcosis

A 2-year-old dog had bilateral chorioretinitis and a cough. Systemic cryptococcosis was diagnosed by evaluating a trans-tracheal aspirate and a cryptococcal latex-particle agglutination antigen titer. Clinical remission was achieved with ketoconazole administration, an imidazole antifungal agent. Serial antigen titers were used to monitor treatment, which was continued for 12 months. Ketoconazole therapy was well tolerated by the dog.     

Kinetic analysis of demethylation of 13C-aminopyrine in healthy dogs

OBJECTIVE: To describe the kinetics of demethylation of 13C-aminopyrine in healthy dogs for use in determining the most appropriate time for collection of blood samples for a 13C-aminopyrine demethylation blood test for evaluation of hepatic function. ANIMALS: 9 healthy dogs. PROCEDURES: A 2-mL baseline blood sample was collected into an evacuated heparinized tube, and 13C-aminopyrine was administered to each dog (2 mg/kg, IV). Additional 2-mL blood samples were collected 15, 30, 45, 60, 75, 90, 105, 120, 135, 150, 180, 240, 300, and 360 minutes after 13C-aminopyrine administration. The CO2 was extracted from blood samples by addition of a strong acid, and the percentage dose of 13CO2 (PCD) in the extracted gas was determined by fractional mass spectrometry. RESULTS: No dogs had gross evidence of adverse effects, and all had an increase in PCD after IV administration of 13C-aminopyrine. The PCD had the least variability among 5 variables used to evaluate hepatic demethylating capacity. Peak PCD was detected at 30 minutes in 1 dog, 45 minutes in 5 dogs, 60 minutes in 2 dogs, and 75 minutes in 1 dog. The mean PCD for the 9 dogs peaked at 45 minutes after 13C-aminopyrine administration. CONCLUSIONS AND CLINICAL RELEVANCE: PCD appears to be the preferable variable for evaluation of hepatic demethylating capacity. Intravenous administration of 13C-aminopyrine leads to a consistent increase in PCD. Mean PCD peaked 45 minutes after administration, suggesting that blood sample collection 45 minutes after 13C-aminopyrine administration may be appropriate for use in estimating hepatic demethylating capacity.     

Treatment of severe chronic digoxin toxicosis in a dog with cardiac disease, using ovine digoxin-specific immunoglobulin G Fab fragments

Severe digoxin toxicosis in a 13-year-old mixed-breed dog with dilated cardiomyopathy was successfully treated with i.v. administration of ovine digoxin-specific IgG Fab fragments. Management of this dog following treatment with Fab fragments was complicated by hypomagnesemia and loss of the positive inotropic effect of digoxin.     

Non-dexamethasone-suppressible, pituitary-dependent hyperadrenocorticism in a dog

A 5-year-old female dog with hyperadrenocorticism was determined to have pituitary-dependent hyperadrenocorticism even though plasma cortisol concentrations were not suppressed after high-dosage dexamethasone administration. The diagnosis was based on a supranormal response of plasma cortisol to ACTH administration and a lack of suppression of plasma cortisol concentration after administration of 0.1 mg of dexamethasone/kg. Although a higher dosage of dexamethasone (1 mg/kg) did not cause suppression of plasma cortisol, plasma ACTH concentrations in the dog were increased above those in clinically normal dogs, supporting a diagnosis of pituitary-dependent hyperadrenocorticism. During treatment with mitotane, the dog became unconscious and died. Necropsy revealed a pituitary tumor that had compressed and displaced the hypothalamus. Although high-dosage dexamethasone suppression tests often are useful in the differential diagnosis of hyperadrenocorticism, a lack of suppression of plasma cortisol does not necessarily exclude pituitary-dependent hyperadrenocorticism.     

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.     

Adverse reactions suggestive of type III hypersensitivity in six healthy dogs given human albumin

CASE DESCRIPTION:6 healthy dogs given human albumin solution as part of a study were examined following development of an immediate hypersensitivity reaction (1 dog) and signs suggestive of a type III hypersensitivity reaction (all 6 dogs). CLINICAL FINDINGS: All 6 dogs were healthy prior to administration of human albumin solution. One dog developed signs of an immediate hypersensitivity reaction, characterized by vomiting and facial edema, during administration of human albumin solution. All 6 dogs developed signs of a delayed adverse reaction 5 to 13 days after administration of human albumin solution. Initial clinical signs included lethargy, lameness, edema, cutaneous lesions indicative of vasculitis, vomiting, and inappetance. TREATMENT AND OUTCOME: In the dog with signs of immediate hypersensitivity, signs resolved after administration of human albumin solution was discontinued and diphenhydramine was administered. Supportive treatment was provided after dogs developed signs of a delayed adverse reaction. Four dogs recovered, but 2 dogs died despite treatment. All 6 dogs were found to have antihuman albumin antibodies. There was no evidence of contamination of the human albumin solution. CLINICAL RELEVANCE: Findings suggest that administration of human albumin solution in healthy dogs with normal serum albumin concentrations may result in signs of a type III hypersensitivity reaction.     

Bee sting envenomation resulting in secondary immune-mediated hemolytic anemia in two dogs

Immune-mediated hemolytic anemia secondary to bee envenomation developed in 2 dogs. Clinical signs included lethargy, hematuria, ataxia, and seizures; 1 dog died. Clinicopathologic data included nonregenerative anemia, spherocytosis, positive results for Coombs' test, and occult hematuria. Treatment included oral administration of corticosteroids at immunosuppressive dosages and supportive care. The surviving dog initially responded to corticosteroids, but hemolysis recurred as the dosage was tapered. Hemolysis resolved with prolonged administration of corticosteroids. Bee venom contains hyaluronidase, histamines, and hemolysins that cause toxic and hemolytic effects. Envenomation should be considered in any dog with hemolytic anemia in which other causes are ruled out and exposure to bees is known.