Background: Primary hyperlipidemia is a condition that affects some specific breeds. It has been previously described in Miniature Shnauzer, Beagles, Shetland Shepdog and West Highland White Terrier. There are no reports of primary hyperlipidemia in Maltese dogs. It is a hereditary disorder of lipoprotein metabolism. The etiology is unknown and may be related to a genetic problem in lipoprotein lipase or to the absence of apaprotein CII. Clinical signs include spontaneous arterosclerosis, retinal lipemia, cutaneous xanthomas, abdominal pain, lethargy, vomiting and / or diarrhea. Neurological manifestations such as seizures and behavioral changes may also occur. The aim of this report is to describe a case of reactive seizures due to hyperlipidemia in a dog.Case: A 5-year-old male Maltese dog was admitted with a history of seizures. Hypertension and abdominal distension with large amounts of intestinal gases were found in general physical examination. Neurological examination revealed impaired nasal septum sensory perception, which was slightly bilaterally reduced, and pain on cervical palpation and in the brachial plexus region. Based on history and clinical examination, it was possible to locate the lesion in the thalamocortical region and to suspect idiopathic epilepsy, reactive seizures, and symptomatic epilepsy due to meningoencephalitis of unknown origin. The diagnosis of primary hyperlipidemia was made by exclusion with the aid of laboratory tests and ultrasound. After the establishment of a fat restriction diet, bezafibrate, phenobarbital, and omega-3 supplementation, the animal improved significantly with the reduction of epileptic seizures.Discussion: The initial clinical suspicion was hyperadrenocorticism as the primary cause of hyperlipidemia. This suspicion was based on the presence of polyphagia, polydipsia, polyuria and abdominal distension, together with laboratory results of thrombocytosis, increased ALT and AF, and hyposenuria; but ultrasound images and ACTH stimulation test ruled out this differential diagnosis. Hypothyroidism was also ruled out since LDL values were normal and the animal was extremely active. Regarding nephrotic syndrome, it was also excluded for some alterations would be present, such as severe proteinuria, cholesterol reduction and hypoalbuminemia. As for diabetes mellitus, it was discarded because of the dog’s young age and due to the absence of suggestive clinical signs. The suspicion of primary hyperlipidemia was based on increased levels of triglycerides, and the presumptive diagnosis was of reactive seizures due to hyperlipidemia. It is essential, when treating hyperlipidemia, to readjust to a low-calorie diet with fat concentration below 8% and protein level above 18%. Generally, these restricted diets are for life. Omega-3 supplementation can be performed to help maintain low levels of triglycerides. Drug therapy is usually carried out with bezafibrate, which is used in human medicine as treatment for hypertriglyceridemia, and has showed good results in the control of hypertriglyceridemia and hypercholesterolemia in dogs with primary and secondary hyperlipidemia. Six months after the beginning of the treatment, the animal no longer presented abdominal distension and pain, cholesterol values and its fractions were controlled, as well as triglycerides. Seizures were also under control. Therefore, hyperlipidemia is an important differential diagnosis in cases of patients presenting seizures, especially when dealing with young animals showing signs of metabolic diseases.

Background: Compulsive disorders are excessive and repetitive behaviors that jeopardize the quality of life of both animal and guardian. It generally affects dogs between 6 and 36 months of age and its etiology is associated to stress, anxiety and genetic predisposition. Clinical manifestations are the usual behaviors of the dog, but overly and inappropriately done. Diagnosis is based on a history of repetitive behavior and on clinical and complementary exams to discard other diseases. The aim of this study is to report a case of compulsive disorder in a female Border Collie dog, including diagnostic and therapeutic approaches. Case: A 5-month-old, female, Border Collie dog was presented to Uberaba's Veterinary Hospital owing to a chasing shadows behavior that started as a playtime activity but intensified to the point of becoming a repetitive and excessive act, followed by self-trauma and excessive barking. Clinical examination showed lesions in nasal planum region. No alterations were observed on neurological examination apart from the chasing of shadows that also happened in the consultation room. Therefore, since there were no other findings on clinical and neurological exams, and since the manifestation occurred as a response to environmental stimuli (presence of shadows), it was established a presumptive diagnosis of compulsive disorder. Treatment with trazodone chlorhydrate was performed, and it was indicated ovariohysterectomy, a follow-up with a professional behaviorist and trainer and environment modifications. After a fortnight, it was observed a discreet improvement of the clinical signs, hence a second anxiolytic, clomipramine, was added to the treatment. Approximately 3 months after the beggining of therapy, there was improvement of the animal's clinical picture, being calmer and most days ignoring the shadows. Discussion: Compulsive disorders are described as exaggerated and repetitive behaviors that jeopardize the animal's interaction with its environment and with its tutor. The animal of this report showed repetitive behavior of chasing shadows, with claw abrasion and self-inflicted nasal lesions caused by leaping and biting on the surfaces where the shadows were projecting. Additionally, during the manifestation of the behavior, the animal barked excessively, which compromised the quality of the guardians' lives. The patient was a Border Collie female dog, though there are no descriptions of this type of behavior in this breed. The starting age of this patient's manifestations is consistent with previous reports, which observed it more frequently in animals with 6 to 36 months of age. The absence of alterations on clinical and neurological exams that could indicate maladies in other systems, in addition to a detailed anamnesis and assessment of videos of the animal recorded in his domicile, enabled the diagnosis of compulsive disorder. Ovariohysterectomy was done with the purpose of reducing the previously mentioned behavior. Drug therapy in addition to behavior training were efficient to promot...

Background: Pulmonary bullae are thin-walled cavitary lesions within the subpleural parenchyma. They are a result of the destruction, dilatation and coalescence of bordering alveoli and their rupture is the most common cause of pneumothorax in dogs. Radiographic and CT imaging are excellent tools for identifying and quantifying pneumothorax. Surgical treatment is considered standard for treatment of pneumothorax consequential to pulmonary bullae. The aim of this report was to describe a case of pneumothorax secondary to pulmonary bullae in a dog.Case: A 5-year-old male crossbreed dog, weighing 11.5 kg, was presented to the Uberaba’s Veterinary Hospital due to becoming easily tired in the previous 3 weeks, and its worsening in the last 2 days by presenting panting. The dog’s guardian did not witness any traumas, but informed that the animal resided with other 14 dogs and also that it frequently collided the thorax against the door when it came down from the bed. Physical examination showed diaphragmatic breathing, inspiratory dyspnea and stridor lung sound. Thoracocentesis revealed presence of air in the pleural cavity and pneumothorax. Radiographic images confirmed this condition. The dog stayed in the hospital and chest drains were placed. Since the amount of sucked air did not reduce with time and due to the emergence of subcutaneous emphysema, the dog went through exploratory thoracotomy that revealed impairment of the right caudal lung lobe, proceeding to lobectomy. The dog stayed in the hospital with chest drains until the contents of the suctions reduced significantly. With the removal of the drains, the dog was sent home and had a full recovery. Histopathology of the impaired lung revealed pulmonary bullae.Discussion: The dog from this report presented clinical signs consistent with pneumothorax, such as dyspnea, diaphragmatic breathing and exercise intolerance. Radiography of the chest region revealed images consistent with this condition, as it is an excellent tool for identifying it. This dog’s guardian was unable to confirm if there was occurrence of trauma due to the large number of cohabitants. In dogs, spontaneous pneumothorax commonly results from the rupture of pulmonary bullae, and these bullae may result from trauma, infectious diseases, thrombosis, obstructive, neoplastic, congenital or idiopathic conditions. Except from trauma, there were no evidence to support any of the other causes of pulmonary bullae in this case.  Traumatic injuries are very common in veterinary medicine, and blunt thoracic traumas with consequential pneumothorax are especially common. The emerging of subcutaneous emphysema, as happened with this dog, is frequently associated with pneumomediastine, and rarely has pathophysiologic impairments. The patient stayed in the hospital for support therapy and thoracocentesis, corroborating with literature; but since there was no improvement, it went through exploratory lobectomy, which revealed impairment of the right caudal lung lobe, proceeding to its exeresis. Surgical intervention is standard procedure in these cases. Histopathology of the impaired lung suggested the presence of pulmonary bullae. In literature, histopathological definitions for this condition are inconsistent, but usually locate the bullae within the pulmonary parenchyma, having walls less than 1 mm thick. Through radiology, unlike with cysts, identifying pulmonary bullae is challenging. In conclusion, this report showed that pulmonary bullae should be considered as a differential diagnose in patients showing pneumothorax considering it is hard to identify through imaging, and that it is important to adopt early therapy and surgical intervention for better outcomes.Keywords: dyspnea, panting, pulmonary lobectomy, thoracotomy, chest drain.Titulo:  Pneumotórax secundário a bolha pulmonar em cão.Descritores: dispneia, ofegante, lobectomia pulmonar, toracotomia, dreno torácico.

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Background: Systemic lupus erythematosus (SLE) is an immune-mediated and multisystemic disorder which etiology is believed to be multifactorial. Its clinical signs vary accordingly to affected organs, cutaneous lesions being the most frequently observed. There are few reports of SLE in dogs with neurological manifestations. Therefore, the aim of this report is to describe a case of SLE in a dog with indicative signs of nervous system involvement.Case: A 6-year-old Border Collie bitch was referred to the Veterinary Hospital (HVU) of the University of Uberaba (UNIUBE) with a history of  with cluster seizures, inappetence and urinary incontinence. Erythema and flaking of nasal plan were noted on physical examination, and splenomegaly on abdominal palpation. Thrombocytopenia and slightly increased ALT were found on blood tests. Ehrlichiosis was suspected and doxycycline was prescribed together with phenobarbital for the control of seizures. In the follow-up visit, the dog was still presenting urinary incontinence, thrombocytopenia and splenomegaly. Also, an ulcer on the nasal mucocutaneous junction was observed. The patient went through a neurological examination which indicated thalamocortical lesion. Cerebrospinal fluid samples were obtained for cytology, culture and canine distemper test, and serology tests for leishmaniasis, toxoplasmosis and neosporosis were done. No alterations were found in these exams. The histopathology of the nasal lesion was proceeded and showed results consistent with lupus erythematosus. It was prescribed a 15-day course of prednisolone at immunosuppressive dose. The patient showed clinical improvement with this treatment. Azathioprine was started along with gradual removal of prednisolone. After twenty days of discontinuation of this drug, the dog presented epileptic seizures, urinary incontinence, thrombocytopenia, increased ALT and worsened nasal lesion. Prednisolone at immunosuppressive dose was reintroduced and the dose of azathioprine, increased. One week past this, the patient showed inappetence and an extensive hematoma in the thoracic region. Lab exams confirmed drug-induced acute pancreatitis. All medications were interrupted, the patient was hospitalized, and treatment for pancreatitis was initiated, but the dog passed away.Discussion: For involving multiple body systems and for presenting varied clinical signs, diagnosing SLE can be challenging in clinical routine. The dog from this report was a Border Collie; this breed is considered to be predisposed to this disease. The animal had a history of being exposed to solar radiation for a large part of the day, had dyspigmentation of nasal plan and had no application of sunscreen, predisposing the occurrence of SLE. Neurological signs are uncommon in SLE, but the seizures and the urinary incontinence were the main reasons for the dog’s guardian to look for medical assistance. The suspicion for SLE was raised due to cutaneous manifestations and persistent thrombocytopenia along with splenomegaly. Histopathological findings are essential for diagnosing SLE, as well as antinuclear antibody tests. Nonetheless, due to financial limitations, this last test was not performed. Azathioprine is an immunomodulating drug largely used along with glucocorticoids when treating SLE; however, this medication is prone to induce side effects as the ones presented by the dog from this report. Therefore, it is concluded that SLE should be considered as a differential diagnosis in patients showing cutaneous, hematological, systemic and neurological manifestations, considering the variety of signs caused by this disorder.Keywords: seizures, dog, immune-mediated encephalopathy. Lúpus eritematoso sistêmico associado a manifestações neurológicas em cadela da raça Border CollieDescritores: crises epilépticas, cão, encefalopatia imunomediada.