Anticoagulant rodenticide toxicosis causing tracheal collapse in 4 small breed dogs.

OBJECTIVE: To describe 4 cases of tracheal narrowing attributed to tracheal mucosal hemorrhage caused by anticoagulant rodenticide toxicity in breeds predisposed to tracheal collapse. CASE SUMMARY: Over the years 2005-2014, 4 dogs were presented for respiratory distress secondary to diffuse tracheal narrowing. All dogs had possible anticoagulant rodenticide ingestion and prolonged prothrombin time. All dogs received fresh-frozen plasma transfusions, vitamin K1 supplementation, and supportive care. Tracheal narrowing improved on follow-up radiographs in 3 of 4 patients. One of 4 did not have follow-up radiographs performed. All dogs survived. NEW OR UNIQUE INFORMATION PROVIDED: Anticoagulant rodenticide toxicity causing clinical signs consistent with tracheal collapse is a rare but recognized phenomenon that has not been previously reported in breeds prone to tracheal collapse.

SAFETY AND TOXICITY OF AN ACCELERATED COARSELY FRACTIONATED RADIATION PROTOCOL FOR TREATMENT OF APPENDICULAR OSTEOSARCOMA IN 14 DOGS: 10 GY × 2 FRACTIONS.

Coarsely fractionated radiation is commonly used as a method for pain control in dogs with appendicular osteosarcoma, however there is little published information on optimal protocols. The aim of this retrospective, descriptive study was to report safety and toxicity findings in a sample of dogs with appendicular osteosarcoma that had been treated with a radiation scheme of 10 Gy delivered over two consecutive days for a total of 20 Gy. Dogs were included in the study if they had osteosarcoma that was treated with the aforementioned protocol. Dogs were excluded if treated with the same protocol for any other bone tumor besides osteosarcoma or inadequate follow-up. Thirteen of the 14 patients received adjuvant therapy with pamidronate and a nonsteroidal anti-inflammatory. Nine dogs received adjuvant chemotherapy with carboplatin after radiation was complete. Within a median of 14 days, 92.8% of dogs subjectively had improved pain control. Median duration of response (DOR) was 80 days (range 20-365). The majority of patients developed VRTOG grade one toxicity, primarily alopecia. Five dogs (35.7%) developed pathologic fracture postradiation treatment. Timing of fracture was variable ranging from 24 to 250 days. This radiation protocol was well tolerated, with minimal toxicity, subjectively improved survival time, and had the benefit of being completed in two consecutive days.

Interstitial pneumonia and pulmonary hypertension associated with suspected ehrlichiosis in a dog.

BACKGROUND: In dogs with canine monocytic ehrlichiosis (CME), respiratory signs are uncommon and clinical and radiographic signs of interstitial pneumonia are poorly described. However, in human monocytic ehrlichiosis, respiratory signs are common and signs of interstitial pneumonia are well known. Pulmonary hypertension (PH) is classified based on the underlying disease and its treatment is aimed at reducing the clinical signs and, if possible, addressing the primary disease process. PH is often irreversible, but can be reversible if it is secondary to a treatable underlying etiology. CME is currently not generally recognized as one of the possible diseases leading to interstitial pneumonia and secondary PH in dogs. Only one case of PH associated with CME has been reported worldwide. CASE PRESENTATION: A seven-year-old, male intact, mixed breed dog was presented with 2 weeks history of lethargy and dyspnea. The dog previously lived in the Cape Verdean islands. Physical examination showed signs of right-sided congestive heart failure and poor peripheral perfusion. Thoracic radiography showed moderate right-sided cardiomegaly with dilation of the main pulmonary artery and a mild diffuse interstitial lung pattern with peribronchial cuffing. Echocardiography showed severe pulmonary hypertension with an estimated pressure gradient of 136 mm Hg. On arterial blood gas analysis, severe hypoxemia was found and complete blood count revealed moderate regenerative anemia and severe thrombocytopenia. A severe gamma hyperglobulinemia was also documented. Serology for Ehrlichia canis was highly positive. Treatment with oxygen supplementation, a typed packed red blood cell transfusion and medical therapy with doxycycline, pimobendan and sildenafil was initiated and the dog improved clinically. Approximately 2 weeks later, there was complete resolution of all clinical signs and marked improvement of the PH. CONCLUSION: This report illustrates that CME might be associated with significant pulmonary disease and should be considered as a possible differential diagnosis in dogs presenting with dyspnea and secondary pulmonary hypertension, especially in dogs that have been in endemic areas. This is important because CME is a treatable disease and its secondary lung and cardiac manifestations may be completely reversible.

Shunting between the CVC and both the azygos vein and thoracic duct in a dog with CTD.

A 5 mo old female rottweiler was referred for evaluation of a suspected congenital heart disease. Clinical signs included anorexia, exercise intolerance, and severe loss of body condition. Clinical examination revealed dyspnea, pale mucous membranes, and weak femoral pulses. Pleural and abdominal effusions and iron deficiency anemia were identified. A distended intrathoracic caudal vena cava (CVC) visible on thoracic radiographs suggested that the modified transudate abdominal effusion was the result of improper venous return to the right side of the heart. Cor triatriatum dexter (CTD) was diagnosed via echocardiography but did not explain all the anomalies detected during a contrast echocardiography. Abnormal communications between the CVC and azygos vein and the CVC and thoracic duct were subsequently identified by abdominal ultrasonography and angiography. Medical management with diuretics, iron supplements, and surgical treatment of CTD resulted in normalization of the respiratory rate, the exercise intolerance, and the anemia. To the authors' knowledge, this is the first reported case of CTD associated with shunts between the CTV and both the azygos vein and thoracic duct in dogs. This report emphasizes the importance of presurgical assessment of concurrent thoracic and abdominal congenital vascular abnormalities.

Cardiogenic hypertrophic osteopathy in a dog with a right-to-left shunting patent ductus arteriosus.

A 5-year-old castrated male Shetland Sheepdog was examined because of progressive bilateral hind limb thickening. Cyanosis of the preputial mucous membranes was evident, whereas the oral mucous membranes had a normal color. A well-structured, palisade-like periosteal reaction with no underlying bone destruction was evident on radiographs of the hind limbs. The radiographic changes were consistent with hypertrophic osteopathy (HO). Severe right-sided cardiomegaly was seen on thoracic radiographs, and a diagnosis of patent ductus arteriosus with right-to-left shunting was made by means of echocardiography and contrast echoaortography. The cyanotic heart disease was believed to be the cause of the HO. Hypertrophic osteopathy has been associated with a number of diseases in animals and humans. In humans, congenital heart defects that cause cyanosis are among the most common causes of HO.

Pretreatment clinical and laboratory evaluation of cats with diabetes mellitus: 104 cases (1992-1994).

OBJECTIVE: To assess pretreatment clinical and laboratory findings in cats with diabetes mellitus and to determine the influence of ketoacidosis on pretreatment findings. DESIGN: Retrospective case series. ANIMALS: 104 cats with diabetes mellitus, 38 of which had ketoacidosis. PROCEDURE: Medical records of cats with diabetes mellitus examined over a 20-month period were reviewed. Cats that had received previous treatment for diabetes mellitus, or for which medical records were incomplete, were excluded from this study. RESULTS: Cats ranged in age from 1 to 19 years (median, 11 years). Male cats were twice as likely to develop diabetes as females. The most common historical signs were polyuria, polydipsia, weight loss, and diminished activity. Anorexia or poor appetite was reported more commonly than polyphagia, especially in cats with ketoacidosis. Diminished activity, anorexia, weakness, and vomiting were all significantly more common in ketoacidotic cats than in nonketoacidotic cats. Forty-four cats were considered thin, and 34 were considered obese. All cats had hyperglycemia and most had hypercholesterolemia and high activities of 1 or more hepatic enzymes. Compared with nonketoacidotic cats, ketoacidotic cats were more likely to have had low serum electrolyte values. All cats had glucosuria and 42 (40.4%) had ketonuria. Baseline serum insulin concentrations were measured in 18 cats and were low or at the low end of the reference range in 14 (77.8%) cats. Serum fructosamine concentration, determined in 22 cats, was high in 20 (90.9%) cats. Twenty-three of the 104 (22.1%) cats had concurrent disease, the most common of which were hyperthyroidism, inflammatory bowel disease, and eosinophilic granuloma complex. CLINICAL IMPLICATIONS: In more than a third of cats, diabetes mellitus is complicated by development of ketoacidosis, which increases the severity of clinical and laboratory abnormalities. Diagnosis of diabetes mellitus is made on the basis of signalment (e.g., middle-aged to old male cats), owner complaints (e.g., polyuria, polydipsia, and weight loss), physical examination findings (e.g., lethargy or muscle wasting), and laboratory findings (e.g., hyperglycemia and glucosuria).

Case report: efficacy of oral carnitine therapy for dilated cardiomyopathy in boxer dogs.

This paper investigates the role of carnitine in the etiology and treatment of dilated cardiomyopathy in boxers. Two boxers were diagnosed as having dilated cardiomyopathy on the basis of clinical presentation, chest radiographs, electrocardiography and echocardiography. In one dog, carnitine was administered at 6.0 g (or approximately 250 mg/kg live weight (LW) daily per os, and this dog remained asymptomatic for 4 mo until it presented for anorexia, coughing and weakness. Necropsy and histologic findings were consistent with boxer cardiomyopathy in both dogs. Cardiac carnitine concentration was 567 nmol/g wet weight in the unsupplemented dog, which is below the normal mean +/- SD concentration of 1493 +/- 141 nmol/g wet weight. Low cardiac carnitine concentrations appear to be a consistent finding for dilated cardiomyopathy in boxers. However, in the dog that received carnitine therapy, cardiac carnitine was 2802 nmol/g wet weight, and all tissues assayed in the supplemented dog had higher carnitine concentrations than normal dogs. Elevation of tissue carnitine failed to ameliorate dilated cardiomyopathy in this dog. Oral carnitine supplementation in these therapeutic doses appears not to resolve dilated cardiomyopathy in all boxers.