Background: The most common location of malignant tumors of the peripheral nerve sheath in the spinal cord is the intradural-extramedullary region, and is rare in the spinal nerve roots in the lumbar region. They mainly affect large female dogs over six years of age. Imaging tests assist in the presumptive diagnosis, but confirmation requires histopathological and immunohistochemical examination. The prognosis is guarded. Diagnostic imaging, anatomopathological and immunohistochemical findings of a malignant tumor of the intradural-extramedullary peripheral nerve sheath with medullary infiltration in the lumbar region in a young dog are reported.Case: A body of a 6-year-old Poodle dog was donated for necropsy and diagnostic clarification. In the history, there was a suspicion of lumbar intramedullary neoplasia, detected by computed tomography (CT), with a 4 years progressive chronic evolution. Additionally, the dog had hidden spina bifida (L7 to S3), as detected by radiography and CT. On post mortem radiographic examination (X-ray), there was an enlargement of the vertebral canal (T10 to S2), intense osteolysis (L1 to S2), spinous processes (L5 to L7), and ankylosis (L3 to L7). Necropsy revealed ankylosis (L3 to L7) and intradural-extramedullary mass (9.5 × 2.6 × 2.3 cm) (L2 to L6). No metastases were identified. On microscopy, there was neoplastic proliferation of cells with intense pleomorphism, arranged in bundles interlaced in palisades and sometimes solid mantles. The mitotic index was high, ranging from 10 to 12 mitoses per field. There was also necrosis, hemorrhage, edema, and focal axonal demyelination of the adjacent white matter in the spinal cord. Masson Trichrome staining highlighted an intense diffuse conjunctive stroma. There was a suspicion of a malignant tumor of the peripheral nerve sheath and an immunohistochemical panel was performed for confirmation. There was strong and diffuse positivity for vimentin and S-100 and partial positivity for neuron-specific enolase (NSE), negative for anti-factor VIII, glial fibrillary acidic protein (GFAP), α-actin for smooth muscle, cytokeratin, neurofilament, and desmin. Thus, the diagnosis of malignant neoplasm of the peripheral nerve sheath was confirmed.Discussion: Peripheral nerve sheath tumors are classified as benign or malignant. In dogs, they are frequent in elderly, females, and large breeds. In this case report, the animal was young, female, and small breed. The location of the spinal nerve roots is uncommon, and is more commonly found in the brachial plexus. In the animal reported, the tumor was observed as lumbar swelling. Clinical signs vary with the affected region, however, neurogenic claudication and muscle atrophy are more frequent, as observed in this report. Imaging examinations such as X-rays and CT assist in the presumptive diagnosis. In this case report, spina bifida was identified on radiography, and CT suggested the presence of intramedullary neoplasia and allowed to monitor tumor growth. Post mortem X-ray imaging revealed intense osteolysis and ankylosis, which were confirmed at necropsy, which also elucidated its intradural-extramedullary location with infiltration into the spinal cord. The confirmation of the neoplasm was made by histopathological and immunohistochemical examination; the latter should be made a panel, not restricted to the use of antibodies S-100 and vimentin only. The prognosis of malignant peripheral nerve sheath tumors (MPNST) of the spinal cord is poor, and although there are palliative methods, there is no curative treatment, as complications can interfere with the quality of life of the animal. MPNST should be included in the differential diagnosis of spinal disorders, even in young dogs and small breeds. CT helps in early diagnosis to make decisions aimed at the animal's well-being.
Background: Peritoneopericardial diaphragmatic hernia is a congenital defect characterized by an anomalous communication between the abdominal cavity and pericardial sac, which can lead to displacement of the abdominal viscera into the thoracic cavity. The occurrence in felines is higher among long-haired breeds, mainly the Persian breed, possibly based onan autosomal recessive inheritance. The diagnosis of PPDH is performed by means of chest radiography with or without contrast, in association with other imaging tests such as ultrasonography and echocardiography. Our objective in this study was to report the occurrence and macroscopic changes in a case of peritoneopericardial diaphragmatic hernia in a Persian feline. Case: A 9-year-old male Persian cat weighing 3.4 kg was referred to the HPET-Private Veterinary Clinic, Salvador, Bahia, with an history of weight loss and chronic intermittent vomiting during the preceding 6 months, with lateral decubitus and breathing difficulties. Ultrasonography revealed findings suggestive of an infiltrative process in the stomach and duodenum, enlarged gastric lymph nodes, and some nodular images indicating slight displacement of the liver. Chest radiography revealed a cardiac silhouette with markedly enlarged dimensions associated with a dorsal deviation of the terminal trachea, and echocardiography revealed a small amount of pericardial effusion. The patient showed initial clinical improvement after blood transfusion; however, after 2 days, he exhibited significant clinical worsening and was therefore euthanized with the owner's consent. Post mortem evaluation revealed partial herniation of the liver and gallbladder into the chest cavity through a diaphragmatic hernia ring. The heart was partially surrounded by the left medial lobe of the liver, which was displaced into the pericardial sac. Herniated hepatic lobes had an irregular capsular surface with evident lobulation and tension lipidosis. In the abdominal cavity, the remainder of the liver (right lateral and medial lobes) was observed to be slightly enlarged, with an irregular surface, diffusely reddish with intense evidence of the lobular pattern and white and firm multifocal areas (fibrosis). In the duodenum, close to the pylorus, there was a nodule measuring 2.8 x 2.5 x 1.0 cm, with a whitish and ulcerated surface. When cut, it was soft and exhibited a homogeneous, whitish compact surface.Histopathological examinationshowed marked proliferation of fibrous connective tissue, which for the most part separated the lobes by septa and surrounded the portal space (fibrosis), a marked diffuse chronic inflammatory infiltrate composed of lymphocytes and plasma cells. In addition, marked bile duct hyperplasia and multifocal areas of fatty degeneration (steatosis).Discussion: The diagnosis was based on the association of clinical and pathological findings. Considering the age and clinical signs presented by the patient in this report, as well as the presence of few radiographic signs that were indicative of PPDH, the first differential diagnosis thought was pericardial neoplasia. Peritoneopericardial diaphragmatic hernia in felines is always of congenital origin and may occur asymptomatically depending on the number and involvement of herniated viscera. In this case, the patient's diagnosis of peritoneopericardial hernia was a necropsy finding; the fact that in agreement with previous reports of high rates of incidental diagnoses reinforces the importance of performing necropsy for confirmation or diagnosis of unexpected pathologies. In the present case, peritoneopericardial diaphragmatic hernia in isolation may not have led to severe anemia that culminated in the patient's death. The anatomopathological findings were compatible with biliary cirrhosis and multifocal liver fibrosis, accompanied by the presence of anemia and consequent hypovolemia. Keywords: congenital diaphragmatic hernia, congenital abnormalities, cats. Título: Hérnia Diafragmática Peritoneopericárdica em um Felino da Raça PersaDescritores: hérnia diafragmática congênita, anomalias congênitas, felinos.
Direitos para esta edição cedidos à Atena Editora pelos autores. Todo o conteúdo deste livro está licenciado sob uma Licença de Atribuição Creative Commons. Atribuição-Não-Comercial-NãoDerivativos 4.0 Internacional (CC BY-NC-ND 4.0). O conteúdo dos artigos e seus dados em sua forma, correção e confiabilidade são de responsabilidade exclusiva dos autores, inclusive não representam necessariamente a posição oficial da Atena Editora. Permitido o download da obra e o compartilhamento desde que sejam atribuídos créditos aos autores, mas sem a possibilidade de alterá-la de nenhuma forma ou utilizá-la para fins comerciais. Todos os manuscritos foram previamente submetidos à avaliação cega pelos pares, membros do Conselho Editorial desta Editora, tendo sido aprovados para a publicação com base em critérios de neutralidade e imparcialidade acadêmica. A Atena Editora é comprometida em garantir a integridade editorial em todas as etapas do processo de publicação, evitando plágio, dados ou resultados fraudulentos e impedindo que interesses financeiros comprometam os padrões éticos da publicação. Situações suspeitas de má conduta científica serão investigadas sob o mais alto padrão de rigor acadêmico e ético.
Gallbladder agenesis is a congenital malformation that is considered extremely rare in dogs. The disease can course asymptomatically or with clinical signs, usually non-specific and including vomiting, anorexia, diarrhea, ascites, and lethargy. The objective of this report was to describe the clinical and anatomopathological aspects of a dog with hepatic encephalopathy secondary to gallbladder agenesis. This condition can be diagnosed during surgery or imaging examinations; however, it is often an incidental finding. In the biochemical examinations, a decrease in alanine aminotransferase and an increase in alkaline phosphatase and hypoalbuminemia were observed. During the necropsy, hepatomegaly was observed with absence of the gallbladder, congestion, cerebral edema, lipiduria, and pulmonary edema. Microscopically, there was intense fibrosis and inflammation in the liver due to chronic cholangiohepatitis (cirrhosis of the liver). The consequence of this lesion secondary to gallbladder agenesis was hepatic encephalopathy. Chronic liver failure exposes the cerebral cortex to toxins that are not metabolized by the liver, such as ammonia, mercaptans, short-chain fatty acids, scatols, indols, and aromatic amino acids. These toxins cause reversible damage to the brain, which results in neurological disorders. In this report, the dog had no clinical neurological signs, and the diagnosis of this condition was observed histologically. Dogs with gallbladder agenesis usually have clinical and pathological findings of hepatobiliary lesions such as cholestasis, cholangiohepatitis, and, in severe cases, hepatic encephalopathy, which are necessary to differentiate from other diseases that affect the hepatobiliary system, such as cholelithiasis, neoplasms, and chronic hepatitis.
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