Congenital extrahepatic portosystemic deviation of gastric vein with azygos in a bitch

Background: Portosystemic shunt (PSS), an alteration commonly found in toy dogs, is caused by an anastomosis between the systemic and portal circulation, interfering with the metabolism of several toxins. It can be of congenital or acquired origin and is classified as intra- or extrahepatic. Clinical signs include the gastrointestinal tract, nervous system, and urinary system according to the fraction of the shunt. It is diagnosed by several imaging tests and exploratory laparotomy. Therapy involves drug therapy and/or surgical correction of the anomalous vessels. Thus, the aim is to present an unusual case of extrahepatic cPSS originating from the left gastric vein and insertion into the azygos vein. Case: A 2-year-old female toy poodle, spayed, weighing 2.7 kg was treated with a history of recurrent cystitis and neurological signs such as focal seizures, ataxia, tremors, blindness, lethargy, head pressing, and compulsive gait. Complementary tests revealed normochromic microcytic anemia, neutrophilia-induced leukocytosis, monocytosis, and lymphopenia. Biochemical analysis revealed hypoproteinemia due to hypoglobulinemia, an increase in alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and gamma-glutamyl transferase, and a decrease in urea. In the urinalysis, ammonium biurate crystals were detected, and Doppler ultrasound revealed microhepathy and the presence of an anomalous gastrosplenic vein inserted into the azygos vein, a finding compatible with the congenital extrahepatic PSS. Abdominal tomography confirmed vascular deviation with a sinuous path originating from the left gastric and splenic veins, inserting into the azygos vein, measuring approximately 5.95 cm in length. Cranial tomography revealed changes consistent with hepatic encephalopathy. Drug therapy was performed with hydration, liver chow, lactulose, probiotics, metronidazole, S-adenosyl-L-methionine, and ursodeoxycholic acid, and after 15 days, surgery was performed to place a 3.5 mm ameroid constrictor ring for gradual occlusion of the anomalous vessel. The animal recovered well, and a control abdominal ultrasound was repeated 30 days after the procedure, noting that the constrictor had not yet fully occluded the deviation. Doppler imaging revealed a favorable evolution with an increase in the diameter of the portal vein in the hepatopetal direction. The patient was followed-up for a year and had a normal and healthy life. Discussion: Extrahepatic PSS is frequently diagnosed in purebred and toy dogs, commonly occurring between the portal vein and one of its tributaries, with a lower frequency of anomalous vessels between the azygos veins, as in the present report. The patient's age and clinical signs were compatible with the disease, in addition to ammonia biurate crystals and hematological and biochemical alterations. The neurological clinical signs observed were compatible with hepatic encephalopathy secondary to congenital PSS. The imaging examinations facilitated the identification of the extrahepatic vascular anomaly, with the tomography being more accurate and helping in proper surgical planning. Clinical treatment should be performed for presurgical stabilization, and occlusion can be performed by placing cellophane bands or an ameroid constrictor, which is the technique of choice for congenital PSS, as it allows for slow constriction to avoid acute portal hypertension, as in this case, emphasizing that anesthesia in animals with portosystemic shunts must be performed with care.

Hepatic encephalopathy in adult dog secondary to cirrhosis due to congenital biliary agenesis: a case report / Encefalopatia hepática em cão adulto secundária a cirrose causada por agenesia biliar congênita: relato de caso

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.

A agenesia de vesícula biliar é uma má formação congênita, considerada extremamente rara em cães. A doença pode cursar de forma assintomática ou com sinais clínicos, geralmente, inespecíficos que incluem vômitos, anorexia, diarreia, ascite e letargia. O objetivo deste relato foi descrever os aspectos clínicos e anatomopatológicos de um cão com encefalopatia hepá-tica secundária a agenesia da vesícula biliar, esta condição pode ser diagnosticada durante uma cirurgia ou exames de imagem, entretanto frequentemente é um achado incidental. Como resultados, nos exames bioquímicos observou-se a diminuição da alanina aminotransferase, aumento da fosfatase alcalina e hipoalbuminemia. Durante a necropsia foi observado hepatomegalia com ausência da vesícula biliar, congestão e edema cerebral, lipidúria e edema pulmonar. Microscopicamente, no fígado havia intensa fibrose e inflamação pela colangiohepatite crônica (cirrose hepática). A consequência desta lesão secundária a agenesia da vesícula biliar, foi a encefalopatia hepática. A insuficiência hepática crônica expõe o córtex cerebral às toxinas não metabo-lizadas pelo fígado, tais como a amônia, mercaptanos, ácidos graxos de cadeia curta, escatóis, indóis e aminoácidos aromáti-cos. Essas toxinas causam danos reversíveis ao encéfalo, o que resulta em distúrbios neurológicos. No presente caso, o cão não apresentou sinais clínicos neurológicos e o diagnóstico desta condição foi observado histologicamente. Cães com agenesia de vesícula biliar, geralmente exibem achados clínicos e patológicos de lesões hepatobiliares, como colestase, conlangiohepatite e, em casos graves, encefalopatia hepática, sendo necessário diferenciar de outras doenças que acometem o sistema hepatobiliar, como colelitíase, neoplasias e hepatites crônicas.

Hepatic encephalopathy in adult dog secondary to cirrhosis due to congenital biliary agenesis: a case report / Encefalopatia hepática em cão adulto secundária a cirrose causada por agenesia biliar congênita: relato de caso

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.(AU)

A agenesia de vesícula biliar é uma má formação congênita, considerada extremamente rara em cães. A doença pode cursar de forma assintomática ou com sinais clínicos, geralmente, inespecíficos que incluem vômitos, anorexia, diarreia, ascite e letargia. O objetivo deste relato foi descrever os aspectos clínicos e anatomopatológicos de um cão com encefalopatia hepá-tica secundária a agenesia da vesícula biliar, esta condição pode ser diagnosticada durante uma cirurgia ou exames de imagem, entretanto frequentemente é um achado incidental. Como resultados, nos exames bioquímicos observou-se a diminuição da alanina aminotransferase, aumento da fosfatase alcalina e hipoalbuminemia. Durante a necropsia foi observado hepatomegalia com ausência da vesícula biliar, congestão e edema cerebral, lipidúria e edema pulmonar. Microscopicamente, no fígado havia intensa fibrose e inflamação pela colangiohepatite crônica (cirrose hepática). A consequência desta lesão secundária a agenesia da vesícula biliar, foi a encefalopatia hepática. A insuficiência hepática crônica expõe o córtex cerebral às toxinas não metabo-lizadas pelo fígado, tais como a amônia, mercaptanos, ácidos graxos de cadeia curta, escatóis, indóis e aminoácidos aromáti-cos. Essas toxinas causam danos reversíveis ao encéfalo, o que resulta em distúrbios neurológicos. No presente caso, o cão não apresentou sinais clínicos neurológicos e o diagnóstico desta condição foi observado histologicamente. Cães com agenesia de vesícula biliar, geralmente exibem achados clínicos e patológicos de lesões hepatobiliares, como colestase, conlangiohepatite e, em casos graves, encefalopatia hepática, sendo necessário diferenciar de outras doenças que acometem o sistema hepatobiliar, como colelitíase, neoplasias e hepatites crônicas.(AU)

Crotalaria spectabilis poisoning in a horse

Plant poisoning is an important cause of death in horses and cattle in Brazil. Crotalaria spp. has stood out in this scenario due to its toxic potential caused by monocrotaline, a pyrrolizidine alkaloid found throughout the plant, mainly in seeds. Here is reported a case of Crotalaria spectabilis poisoning a horse. A horse consumed oats contaminated with Crotalaria spectabilis seed and presented clinical signs of toxicosis characterized by jaundice, progressive weight loss, hemoglobinuria, subcutaneous edema in the pectoral region and neurological symptoms typical of hepatic encephalopathy. In the serum evaluation, there was an increase in the activity of the enzymes alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT) and aspartate transaminase (AST), urea, creatinine and creatine phosphokinase (CPK). At necropsy, the main macroscopic findings were opaque and congested liver with capsular irregularity and accentuated the lobular pattern, trachea with foamy and pinkish fluid and congested and edematous pulmonary lobes. The main histopathological findings were hepatic fibrosis, periportal ductal hyperplasia, centrilobular necrosis, megalocytosis and binucleated hepatocytes. The brain parenchyma showed perivascular edema and Alzheimer type II astrocytes. Crotalaria spp. is among the main plants that cause acute or chronic mortality after exposure to the toxic compound in horses and farm animals.(AU)

Crotalaria spectabilis poisoning in a horse

Plant poisoning is an important cause of death in horses and cattle in Brazil. Crotalaria spp. has stood out in this scenario due to its toxic potential caused by monocrotaline, a pyrrolizidine alkaloid found throughout the plant, mainly in seeds. Here is reported a case of Crotalaria spectabilis poisoning a horse. A horse consumed oats contaminated with Crotalaria spectabilis seed and presented clinical signs of toxicosis characterized by jaundice, progressive weight loss, hemoglobinuria, subcutaneous edema in the pectoral region and neurological symptoms typical of hepatic encephalopathy. In the serum evaluation, there was an increase in the activity of the enzymes alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT) and aspartate transaminase (AST), urea, creatinine and creatine phosphokinase (CPK). At necropsy, the main macroscopic findings were opaque and congested liver with capsular irregularity and accentuated the lobular pattern, trachea with foamy and pinkish fluid and congested and edematous pulmonary lobes. The main histopathological findings were hepatic fibrosis, periportal ductal hyperplasia, centrilobular necrosis, megalocytosis and binucleated hepatocytes. The brain parenchyma showed perivascular edema and Alzheimer type II astrocytes. Crotalaria spp. is among the main plants that cause acute or chronic mortality after exposure to the toxic compound in horses and farm animals.

Anestesia para correção de shunt portossistêmico com anel de ameróide em cão / Anesthesia for the correction of portosystemic shunt with an ameroid ring in a dog

O shunt ou desvio portossistêmico (DPS) é uma conexão anormal entre a circulação portal e sistêmica, que desvia o fluxo sanguíneo do fígado em variados graus. Nesse contexto, uma anestesia de qualidade e segura faz toda diferença na recuperação do paciente. Com isso, o presente trabalho teve o objetivo de relatar a técnica anestésica utilizada para o tratamento cirúrgico de um caso de shunt portossistêmico congênito em um cão da raça Yorkshire Terrier, fêmea, de quatro anos, pesando aproximadamente quatro quilos, que apresentava sintomas neurológicos decorrentes de encefalopatia hepática, devido à DPS. Para a medicação pré-anestésica (MPA), foi utilizado o cloridrato de remifentanila (2mg), na taxa de 10µg/Kg/h. Propofol (1%) foi utilizado para indução anestésica, na dose de 1mg/Kg/min, e para anestesia periglótica foi usado cloridrato de lidocaína (2%), no volume de 0,1mL/Kg. Quanto à manutenção anestésica, foi utilizado isoflurano (100%), em um vaporizador universal, citrato de maropitant (1%) em infusão contínua, na taxa de 30µg/Kg/h, cloridrato de remifentanila (2%), na mesma taxa utilizada na MPA, cetamina (10%), na taxa de 0,6mg/Kg/h, e brometo de rocurônio (10mg/mL), na dose de 0,15mg/Kg. Antes do início da cirurgia, foi realizado um bloqueio intraperitoneal com cloridrato de ropivacaína (0,4mg/Kg) diluída em 0,4mL/Kg, na dose de 0,1mL/Kg. Durante todo o procedimento cirúrgico, não houveram intercorrências nem alterações nos parâmetros fisiológicos. Dessa forma, pôde-se observar a eficácia da técnica anestésica utilizada para correção de shunt portossistêmico em um cão apresentando sintomatologia neurológica.

Shunt or portosystemic deviation (DPS) is an abnormal connection between portal and systemic circulation that diverts blood flow from the liver to varying degrees. In this context, quality and safe anesthesia makes all the difference in the patient's recovery. Thus, the present study aims to report the anesthetic technique used for the surgical treatment of a case of congenital portosystemic shunt in a four-year-old Yorkshire Terrier dog, weighing approximately four kilograms, which presented neurological symptoms resulting from of hepatic encephalopathy due to DPS. For pre-anesthetic medication (MPA), remifentanil hydrochloride (2mg) was used at a rate of 10µg/Kg/h. Propofol (1%) was used for anesthetic induction at a dose of 1mg/kg/min and for periglotic anesthesia lidocaine hydrochloride (2%) in a volume of 0.1mL/kg was used. As for anesthetic maintenance, isoflurane (100%) in a universal vaporizer, maropitant citrate (1%) in continuous infusion, at the rate of 30µg/Kg/h, remifentanil hydrochloride (2%), at the same rate used in MPA, ketamine (10%) at a rate of 0.6mg/kg/h and rocuronium bromide (10mg/mL), at a dose of 0.15mg/kg. Before the start of surgery, an intraperitoneal block was performed with ropivacaine hydrochloride (0.4mg/kg) diluted in 0.4mL/kg, in the dose of 0.1mL/kg. Throughout the surgical procedure, there were no complications or changes in physiological parameters. Thus, it was possible to observe the effectiveness of the anesthetic technique used to correct portosystemic shunt in a dog presenting neurological symptoms.

Anestesia para correção de shunt portossistêmico com anel de ameróide em cão / Anesthesia for the correction of portosystemic shunt with an ameroid ring in a dog

O shunt ou desvio portossistêmico (DPS) é uma conexão anormal entre a circulação portal e sistêmica, que desvia o fluxo sanguíneo do fígado em variados graus. Nesse contexto, uma anestesia de qualidade e segura faz toda diferença na recuperação do paciente. Com isso, o presente trabalho teve o objetivo de relatar a técnica anestésica utilizada para o tratamento cirúrgico de um caso de shunt portossistêmico congênito em um cão da raça Yorkshire Terrier, fêmea, de quatro anos, pesando aproximadamente quatro quilos, que apresentava sintomas neurológicos decorrentes de encefalopatia hepática, devido à DPS. Para a medicação pré-anestésica (MPA), foi utilizado o cloridrato de remifentanila (2mg), na taxa de 10µg/Kg/h. Propofol (1%) foi utilizado para indução anestésica, na dose de 1mg/Kg/min, e para anestesia periglótica foi usado cloridrato de lidocaína (2%), no volume de 0,1mL/Kg. Quanto à manutenção anestésica, foi utilizado isoflurano (100%), em um vaporizador universal, citrato de maropitant (1%) em infusão contínua, na taxa de 30µg/Kg/h, cloridrato de remifentanila (2%), na mesma taxa utilizada na MPA, cetamina (10%), na taxa de 0,6mg/Kg/h, e brometo de rocurônio (10mg/mL), na dose de 0,15mg/Kg. Antes do início da cirurgia, foi realizado um bloqueio intraperitoneal com cloridrato de ropivacaína (0,4mg/Kg) diluída em 0,4mL/Kg, na dose de 0,1mL/Kg. Durante todo o procedimento cirúrgico, não houveram intercorrências nem alterações nos parâmetros fisiológicos. Dessa forma, pôde-se observar a eficácia da técnica anestésica utilizada para correção de shunt portossistêmico em um cão apresentando sintomatologia neurológica.(AU)

Shunt or portosystemic deviation (DPS) is an abnormal connection between portal and systemic circulation that diverts blood flow from the liver to varying degrees. In this context, quality and safe anesthesia makes all the difference in the patient's recovery. Thus, the present study aims to report the anesthetic technique used for the surgical treatment of a case of congenital portosystemic shunt in a four-year-old Yorkshire Terrier dog, weighing approximately four kilograms, which presented neurological symptoms resulting from of hepatic encephalopathy due to DPS. For pre-anesthetic medication (MPA), remifentanil hydrochloride (2mg) was used at a rate of 10µg/Kg/h. Propofol (1%) was used for anesthetic induction at a dose of 1mg/kg/min and for periglotic anesthesia lidocaine hydrochloride (2%) in a volume of 0.1mL/kg was used. As for anesthetic maintenance, isoflurane (100%) in a universal vaporizer, maropitant citrate (1%) in continuous infusion, at the rate of 30µg/Kg/h, remifentanil hydrochloride (2%), at the same rate used in MPA, ketamine (10%) at a rate of 0.6mg/kg/h and rocuronium bromide (10mg/mL), at a dose of 0.15mg/kg. Before the start of surgery, an intraperitoneal block was performed with ropivacaine hydrochloride (0.4mg/kg) diluted in 0.4mL/kg, in the dose of 0.1mL/kg. Throughout the surgical procedure, there were no complications or changes in physiological parameters. Thus, it was possible to observe the effectiveness of the anesthetic technique used to correct portosystemic shunt in a dog presenting neurological symptoms.(AU)

Abordagem clínico-cirúrgica de desvio portossistêmico congênito em pequenos animais: quais as novidades? / Clinical and surgical approach of congenital portosystemic shunt in small animals: are there new informations?

Foi realizada uma revisão sobre a fisiopatogenia, sinais clínicos, diagnóstico e principais tratamentos e técnicas para o desvio portossistêmico em pequenos animais. As fontes pesquisadas foram: CAB, MEDILINE por um período retrospectivo de 20 anos e acervos da Biblioteca da Faculdade de Medicina Veterinária e Zootecnia (FMVZ) da Universidade de São Paulo (USP). O desvio portossistêmico congênito (DPSC) é uma das anormalidades vasculares mais comuns em cães, as raças de pequeno porte apresentam maior incidência. Os DPSCs em cães e gatos são comunicações vasculares que ocorrem do sistema venoso portal para o sistema venoso sistêmico, ou seja, fazem uma via secundária. Há dois tipos de DPSCs, intra-hepático e extra-hepático, observados com frequência em raças de grande porte e miniaturas, respectivamente. O diagnóstico é baseado no histórico de animais jovens com retardo de crescimento, letargia, convulsão ou distúrbio de comportamento principalmente após alimentação, retorno demorado de anestesia ou sedação, crise de encefalopatia hepática, em raças predispostas. A confirmação do vaso anômalo é realizada pela ultrassonografia com doppler, angiografia por tomografia computadorizada ou por ressonância magnética.(AU)

It was performed a review of pathophysiology, clinical signs, diagnostic and main treatments and techniques for portosystemic shunts in small animals. The researched Sources were: a 20 years retrospective research of CAB, MEDILINE and collection of Faculty of MedicineVeterinary and Animal Science (FMVZ) of the Universidade de São Paulo (USP). Congenital portossystemic shunts (CPSS) are one of the vascular abnormalities more common in dogs. Small breeds are the most affected. The CPSS in dogs and cats, are vascular communications between portal venous system and systemic venous system, in other words, a secondary via. There are two types of CPSS, the intrahepatic and extrahepatic shunts, observed in large and small breeds, respectively. The diagnosis is based on clinical findings of young dogs referring delayed development, lethargy, convulsions, behavior disturbances mainly after food ingestion, poor recovery after anesthesia or sedation, hepatic encephalopathy crisis observed breeds with predisposition. Definitive diagnosis of CPSS is done by abdominal doppler ultrasonography, computed tomography angiography or magnetic resonance. Medical management can alleviate signs of hepatic encephalopathy. However, long term treatment is questionable because blood circulation is still bypassing liver to systemic circulation, leading to disturbance of hepatotropic factors distribution to the liver, resulting in liver atrophy. The only definitive treatment is the surgical one. The ideal technique is the progressive attenuation of anomalous vessel and avoid acute portal hypertension. Within the described techniques for surgical treatment, the use of ameroid constrictor represents the safest way of vessel closure. On the other way, some CPS patients can suffer severe perioperative complications. So they need specific clinical and surgical approaches associated to precise image diagnostic to correct localization of the anomalous vessel and surgical success.(AU)

Abordagem clínico-cirúrgica de desvio portossistêmico congênito em pequenos animais: quais as novidades? / Clinical and surgical approach of congenital portosystemic shunt in small animals: are there new informations?

Foi realizada uma revisão sobre a fisiopatogenia, sinais clínicos, diagnóstico e principais tratamentos e técnicas para o desvio portossistêmico em pequenos animais. As fontes pesquisadas foram: CAB, MEDILINE por um período retrospectivo de 20 anos e acervos da Biblioteca da Faculdade de Medicina Veterinária e Zootecnia (FMVZ) da Universidade de São Paulo (USP). O desvio portossistêmico congênito (DPSC) é uma das anormalidades vasculares mais comuns em cães, as raças de pequeno porte apresentam maior incidência. Os DPSCs em cães e gatos são comunicações vasculares que ocorrem do sistema venoso portal para o sistema venoso sistêmico, ou seja, fazem uma via secundária. Há dois tipos de DPSCs, intra-hepático e extra-hepático, observados com frequência em raças de grande porte e miniaturas, respectivamente. O diagnóstico é baseado no histórico de animais jovens com retardo de crescimento, letargia, convulsão ou distúrbio de comportamento principalmente após alimentação, retorno demorado de anestesia ou sedação, crise de encefalopatia hepática, em raças predispostas. A confirmação do vaso anômalo é realizada pela ultrassonografia com doppler, angiografia por tomografia computadorizada ou por ressonância magnética.

It was performed a review of pathophysiology, clinical signs, diagnostic and main treatments and techniques for portosystemic shunts in small animals. The researched Sources were: a 20 years retrospective research of CAB, MEDILINE and collection of Faculty of MedicineVeterinary and Animal Science (FMVZ) of the Universidade de São Paulo (USP). Congenital portossystemic shunts (CPSS) are one of the vascular abnormalities more common in dogs. Small breeds are the most affected. The CPSS in dogs and cats, are vascular communications between portal venous system and systemic venous system, in other words, a secondary via. There are two types of CPSS, the intrahepatic and extrahepatic shunts, observed in large and small breeds, respectively. The diagnosis is based on clinical findings of young dogs referring delayed development, lethargy, convulsions, behavior disturbances mainly after food ingestion, poor recovery after anesthesia or sedation, hepatic encephalopathy crisis observed breeds with predisposition. Definitive diagnosis of CPSS is done by abdominal doppler ultrasonography, computed tomography angiography or magnetic resonance. Medical management can alleviate signs of hepatic encephalopathy. However, long term treatment is questionable because blood circulation is still bypassing liver to systemic circulation, leading to disturbance of hepatotropic factors distribution to the liver, resulting in liver atrophy. The only definitive treatment is the surgical one. The ideal technique is the progressive attenuation of anomalous vessel and avoid acute portal hypertension. Within the described techniques for surgical treatment, the use of ameroid constrictor represents the safest way of vessel closure. On the other way, some CPS patients can suffer severe perioperative complications. So they need specific clinical and surgical approaches associated to precise image diagnostic to correct localization of the anomalous vessel and surgical success.

Cerebrospinal fluid analysis in 58 ruminants showing neurological disorders / Análise do líquido cefalorraquidiano em 58 ruminantes com distúrbios neurológicos

Ruminants may be affected by a wide variety of central nervous system (CNS) diseases. Cerebrospinal fluid (CSF) analysis forms the basis for ante mortem diagnostic evaluation of ruminants with clinical signs involving the CNS. Despite its importance as a tool to aid diagnosis, data regarding CSF examinations in spontaneous cases of CNS diseases in ruminants from Brazil are limited, and most reports involve experimental studies. Therefore, this study aimed to report the results of CSF analysis in 58 ruminants showing signs of neurological disorders. CSF samples for analysis were obtained from 32 cattle, 20 sheep, and 6 goats by cerebello-medullary cistern (n=54) or lumbosacral space (n=4) puncture. These ruminants showed neurological signs related to viral (n=13), mycotic (n=3), or bacterial (n=15) infections, and toxic (n=21), traumatic (n=4), or congenital disorders (n=2). CSF analysis from ruminants with viral infections presented lymphocytic pleocytosis, even though CSF showed no changes in several cases of rabies. Neutrophilic pleocytosis, cloudiness, presence of fibrin clots, and abnormal coloration were evident in the CSF of most cases of CNS bacterial infection, such as meningoencephalitis, meningitis, abscesses, myelitis, and a case of conidiobolomycosis. On the other hand, CSF was unchanged in most cases of toxic disorders, as botulism and hepatic encephalopathy. Elevated CSF density was observed in 60% of ruminants diagnosed with polioencephalomalacia. Our findings show that evaluation of CSF is a valuable diagnostic tool when used in association with epidemiological, clinical and pathological findings for diagnosis of CNS diseases in ruminants.(AU)

Os ruminantes podem ser afetados por uma grande variedade de doenças do sistema nervoso central (SNC). A análise do líquido cefalorraquidiano (LCR) constitui a base da avaliação diagnóstica ante mortem de ruminantes com sinais clínicos envolvendo o SNC. Apesar de sua importância como ferramenta para auxiliar no diagnóstico, os dados referentes aos exames do LCR em casos espontâneos de doenças do SNC em ruminantes no Brasil são limitados, e, a maioria dos relatos envolve estudos experimentais. Portanto, este trabalho teve como objetivo relatar os resultados da análise do LCR em 58 ruminantes com distúrbios neurológicos. Amostras do LCR foram obtidas de 32 bovinos, 20 ovinos e 6 caprinos por punção da cisterna cerebelo-medular (n=54) ou espaço lombossacro (n=4) para posterior análise. Esses ruminantes apresentaram sinais neurológicos relacionados a infecções virais (n=13), micóticas (n=3) ou bacterianas (n=15), e desordens tóxicas (n=21), traumáticas (n=4) ou congênitas (n=2) A análise do LCR de ruminantes com infecções virais apresentou pleocitose linfocítica, embora, em vários casos de raiva, o LCR não tenha apresentado alterações. Pleocitose neutrofílica, turbidez, presença de coágulos de fibrina e coloração anormal foram evidentes no LCR da maioria dos casos de infecções bacterianas do SNC, como meningoencefalites, meningites, abscessos, mielite e um caso de conidiobolomicose. Por outro lado, o LCR não foi alterado na maioria dos casos dos distúrbios tóxicos, como botulismo e encefalopatia hepática. A densidade elevada no LCR foi observada em 60% dos ruminantes diagnosticados com polioencefalomalácia. Nossos resultados mostram que a avaliação do LCR é uma valiosa ferramenta de diagnóstico, quando usada em associação com os achados epidemiológicos, clínicos e patológicos para o diagnóstico de doenças do SNC em ruminantes.(AU)

Cerebrospinal fluid analysis in 58 ruminants showing neurological disorders / Análise do líquido cefalorraquidiano em 58 ruminantes com distúrbios neurológicos

Ruminants may be affected by a wide variety of central nervous system (CNS) diseases. Cerebrospinal fluid (CSF) analysis forms the basis for ante mortem diagnostic evaluation of ruminants with clinical signs involving the CNS. Despite its importance as a tool to aid diagnosis, data regarding CSF examinations in spontaneous cases of CNS diseases in ruminants from Brazil are limited, and most reports involve experimental studies. Therefore, this study aimed to report the results of CSF analysis in 58 ruminants showing signs of neurological disorders. CSF samples for analysis were obtained from 32 cattle, 20 sheep, and 6 goats by cerebello-medullary cistern (n=54) or lumbosacral space (n=4) puncture. These ruminants showed neurological signs related to viral (n=13), mycotic (n=3), or bacterial (n=15) infections, and toxic (n=21), traumatic (n=4), or congenital disorders (n=2). CSF analysis from ruminants with viral infections presented lymphocytic pleocytosis, even though CSF showed no changes in several cases of rabies. Neutrophilic pleocytosis, cloudiness, presence of fibrin clots, and abnormal coloration were evident in the CSF of most cases of CNS bacterial infection, such as meningoencephalitis, meningitis, abscesses, myelitis, and a case of conidiobolomycosis. On the other hand, CSF was unchanged in most cases of toxic disorders, as botulism and hepatic encephalopathy. Elevated CSF density was observed in 60% of ruminants diagnosed with polioencephalomalacia. Our findings show that evaluation of CSF is a valuable diagnostic tool when used in association with epidemiological, clinical and pathological findings for diagnosis of CNS diseases in ruminants.(AU)

Os ruminantes podem ser afetados por uma grande variedade de doenças do sistema nervoso central (SNC). A análise do líquido cefalorraquidiano (LCR) constitui a base da avaliação diagnóstica ante mortem de ruminantes com sinais clínicos envolvendo o SNC. Apesar de sua importância como ferramenta para auxiliar no diagnóstico, os dados referentes aos exames do LCR em casos espontâneos de doenças do SNC em ruminantes no Brasil são limitados, e, a maioria dos relatos envolve estudos experimentais. Portanto, este trabalho teve como objetivo relatar os resultados da análise do LCR em 58 ruminantes com distúrbios neurológicos. Amostras do LCR foram obtidas de 32 bovinos, 20 ovinos e 6 caprinos por punção da cisterna cerebelo-medular (n=54) ou espaço lombossacro (n=4) para posterior análise. Esses ruminantes apresentaram sinais neurológicos relacionados a infecções virais (n=13), micóticas (n=3) ou bacterianas (n=15), e desordens tóxicas (n=21), traumáticas (n=4) ou congênitas (n=2) A análise do LCR de ruminantes com infecções virais apresentou pleocitose linfocítica, embora, em vários casos de raiva, o LCR não tenha apresentado alterações. Pleocitose neutrofílica, turbidez, presença de coágulos de fibrina e coloração anormal foram evidentes no LCR da maioria dos casos de infecções bacterianas do SNC, como meningoencefalites, meningites, abscessos, mielite e um caso de conidiobolomicose. Por outro lado, o LCR não foi alterado na maioria dos casos dos distúrbios tóxicos, como botulismo e encefalopatia hepática. A densidade elevada no LCR foi observada em 60% dos ruminantes diagnosticados com polioencefalomalácia. Nossos resultados mostram que a avaliação do LCR é uma valiosa ferramenta de diagnóstico, quando usada em associação com os achados epidemiológicos, clínicos e patológicos para o diagnóstico de doenças do SNC em ruminantes.(AU)

Hepatic encephalopathy secondary to chronic liver lesions caused by Crotalaria incana in a bovine

Background: Crotalaria spp. Poisoning induces liver or pulmonary disease. C. mucronata, C. juncea, C. spectabilis, andC. retusa are the Crotalaria spp. inducing spontaneous intoxication in livestock in Brazil. C. mucronata and C. junceaare associated with interstitial pneumonia, while C. retusa and C. specatabilis induce hepatotoxicosis. The toxic principle in Crotalaria spp. are dehydropyrrolizidine alkaloids and their N-oxides. C. incana poisoning to livestock is rarelydocumented. This paper reports the clinical signs and pathological findings of a case of Crotalaria incana poisoning in asteer. The chemical finding of a potential toxic dehydropyrrolizidine alkaloid in the plant is documented for the first time.Case: The affected bovine was part of a herd of 80 two-year-old steers that were transferred from Property 1 to Property2, 30 days prior to the event. In the pasture of Property I - where the steers were held for 6 months - there was a heavyinfestation by a Crotalaria species with signs of being consumed by the steers. The plant was identified as Crotalariaincana at the Botanical Laboratory of the Federal University of Mato Grosso do Sul and a voucher specimen was filedthere under the register GCMS 51169. Two days after entering Property 2 one of the steers became depressed, staggering,and in poor body condition. With time, the steer became oblivious to the environment and died 20 days after the onset ofthe clinical signs. Significant necropsy findings were limited to the liver which was markedly enlarged and with roundededges. The hepatic cut surface was mottled with dark red and extensive orange areas of discoloration. The gallbladder wasdistended and the bile was inspissated. Microscopically, in the liver, there was fibrosis, bile duct hyperplasia and hepatocellular megalocytosis. The Glisson’s capsule was markedly thickened by fibrosis. In the brain, there was vacuolation ofmyelin...

Hepatic encephalopathy secondary to chronic liver lesions caused by Crotalaria incana in a bovine

Background: Crotalaria spp. Poisoning induces liver or pulmonary disease. C. mucronata, C. juncea, C. spectabilis, andC. retusa are the Crotalaria spp. inducing spontaneous intoxication in livestock in Brazil. C. mucronata and C. junceaare associated with interstitial pneumonia, while C. retusa and C. specatabilis induce hepatotoxicosis. The toxic principle in Crotalaria spp. are dehydropyrrolizidine alkaloids and their N-oxides. C. incana poisoning to livestock is rarelydocumented. This paper reports the clinical signs and pathological findings of a case of Crotalaria incana poisoning in asteer. The chemical finding of a potential toxic dehydropyrrolizidine alkaloid in the plant is documented for the first time.Case: The affected bovine was part of a herd of 80 two-year-old steers that were transferred from Property 1 to Property2, 30 days prior to the event. In the pasture of Property I - where the steers were held for 6 months - there was a heavyinfestation by a Crotalaria species with signs of being consumed by the steers. The plant was identified as Crotalariaincana at the Botanical Laboratory of the Federal University of Mato Grosso do Sul and a voucher specimen was filedthere under the register GCMS 51169. Two days after entering Property 2 one of the steers became depressed, staggering,and in poor body condition. With time, the steer became oblivious to the environment and died 20 days after the onset ofthe clinical signs. Significant necropsy findings were limited to the liver which was markedly enlarged and with roundededges. The hepatic cut surface was mottled with dark red and extensive orange areas of discoloration. The gallbladder wasdistended and the bile was inspissated. Microscopically, in the liver, there was fibrosis, bile duct hyperplasia and hepatocellular megalocytosis. The Glissons capsule was markedly thickened by fibrosis. In the brain, there was vacuolation ofmyelin... (AU)

Encefalopatia hepática em Amazona aestiva / Hepatic encephalopathy in Amazonas aestiva

A Turquoise-fronted Parrot (Amazona aestiva) was attended at the Veterinary Hospital Dr. Jerônimo Dix-Huit Rosado Maia - HOVET UFERSA presenting changes suggestive of hepatic, apathetic disease, below-average body score and with diarrhea. After correction of the diet and initial treatment with anti-inflammatory and essential amino acids, the animal returned with episodes of seizures, suggesting clinical diagnosis for hepatic encephalopathy. Treatment with silymarin (at a dose of 75 mg / kg orally -VO) twice daily (BID) was instituted for 30 days, then extended for continuous use, thus achieving a stability in the general picture of the animal.

Encefalopatia hepática em Amazona aestiva / Hepatic encephalopathy in Amazonas aestiva

A Turquoise-fronted Parrot (Amazona aestiva) was attended at the Veterinary Hospital Dr. Jerônimo Dix-Huit Rosado Maia - HOVET UFERSA presenting changes suggestive of hepatic, apathetic disease, below-average body score and with diarrhea. After correction of the diet and initial treatment with anti-inflammatory and essential amino acids, the animal returned with episodes of seizures, suggesting clinical diagnosis for hepatic encephalopathy. Treatment with silymarin (at a dose of 75 mg / kg orally -VO) twice daily (BID) was instituted for 30 days, then extended for continuous use, thus achieving a stability in the general picture of the animal.(AU)

Encefalopatia hepática em periquito-da-caatinga causado por manejo nutricional inadequado / Hepatic encephalopathy in a Cactus Parakeet caused by inadequate nutritional management

This is a case report of an early stage hepatic encephalopathy in a Eupsittula cactorum caused by inadequate nutritional management. The clinical suspicion was originated from the anamnesis and the clinical signs of the bird. Blood samples were collected for hemoparasites analysis, complete blood count and uric acid, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) dosages. The treatment prescribed was the administration of hepatoprotective drugs and antibiotics combined with the dietary adequacy in order to reverse the clinical picture.

Encefalopatia hepática em periquito-da-caatinga causado por manejo nutricional inadequado / Hepatic encephalopathy in a Cactus Parakeet caused by inadequate nutritional management

This is a case report of an early stage hepatic encephalopathy in a Eupsittula cactorum caused by inadequate nutritional management. The clinical suspicion was originated from the anamnesis and the clinical signs of the bird. Blood samples were collected for hemoparasites analysis, complete blood count and uric acid, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) dosages. The treatment prescribed was the administration of hepatoprotective drugs and antibiotics combined with the dietary adequacy in order to reverse the clinical picture.(AU)

Encefalopatia hepática secundária à intoxicação por Tephrosia cinerea em ovinos / Hepatic encephalopathy secondary to poisoning by Tephrosia cinerea in sheep

A intoxicação por Tephrosia cinerea causa fibrose hepática periacinar em ovinos na região semiárida do Nordeste, com quadro clínico de ascite acentuada, e, ocasionalmente, com sinais neurológicos. Neste trabalho foram estudadas 16 ovinos em 6 surtos de intoxicação por T. cinerea. Todos os ovinos apresentaram lesões histológicas de fibrose periacinar e seis apresentaram, no encéfalo, vacuolização da substância branca e da junção entre a substância branca e a cinzenta com presença de astrócitos de Alzheimer tipo II na substância cinzenta. A doença foi reproduzida experimentalmente em dois ovinos que apresentaram ascite, desvios vasculares (shunts) porto-sistêmicos e sinais nervosos com lesões histológicas semelhantes a dos casos espontâneos. Na técnica de imuno-histoquímica houve marcação fraca ou ausente do citoplasma astrocitário para o anticorpo anti-GFAP em seis ovinos evidenciando uma alteração degenerativa, em que os astrócitos acumulam corpos densos e reduzem o volume de GFAP. Houve marcação positiva para o anticorpo anti-S100 em oito ovinos, incluindo os dois ovinos experimentais o que sugere reatividade celular, com proliferação mitocondrial e de retículo endoplasmático liso. Estas alterações são caraterísticas dos efeitos da amônia nos astrócitos. Conclui-se que na intoxicação por T. cinerea em alguns ovinos ocorrem sinais nervosos em consequência da encefalopatia hepática.(AU)

In the semiarid region of northeastern Brazil, Tephrosia cinerea causes periacinar hepatic fibrosis in sheep with severe ascites and, occasionally, nervous signs. Sixteen sheep from six outbreaks of T. cinerea poisoning were studied. All sheep had histologic lesion of periacinar fibrosis and six showed, in the brain, vacuolization (spongy degeneration) of the white matter and junction between grey and white matter and presence of Alzheimer type II astrocytes in the grey matter. The disease was produced experimentally in two sheep, that presented porto-sistemic shunts and similar histologic lesions as those observed in the spontaneous cases. Immunohistochemistry revealed weak labelling with anti-GFAP antibodies suggesting a degenerative alteration of astrocytes with accumulation of dense bodies and reduction of the GFAP. There was strong labelling with anti-S100 antibodies suggesting cellular reactivity with proliferation of mitochondria and endoplasmatic reticulum. Such alterations are characteristic of the effects caused by ammonia on the astrocytes. It is concluded that in poisoning by T. cinerea nervous signs due to hepatic encephalopathy occur in some sheep.(AU)

Encefalopatia hepática secundária à intoxicação por Tephrosia cinerea em ovinos / Hepatic encephalopathy secondary to poisoning by Tephrosia cinerea in sheep

A intoxicação por Tephrosia cinerea causa fibrose hepática periacinar em ovinos na região semiárida do Nordeste, com quadro clínico de ascite acentuada, e, ocasionalmente, com sinais neurológicos. Neste trabalho foram estudadas 16 ovinos em 6 surtos de intoxicação por T. cinerea. Todos os ovinos apresentaram lesões histológicas de fibrose periacinar e seis apresentaram, no encéfalo, vacuolização da substância branca e da junção entre a substância branca e a cinzenta com presença de astrócitos de Alzheimer tipo II na substância cinzenta. A doença foi reproduzida experimentalmente em dois ovinos que apresentaram ascite, desvios vasculares (shunts) porto-sistêmicos e sinais nervosos com lesões histológicas semelhantes a dos casos espontâneos. Na técnica de imuno-histoquímica houve marcação fraca ou ausente do citoplasma astrocitário para o anticorpo anti-GFAP em seis ovinos evidenciando uma alteração degenerativa, em que os astrócitos acumulam corpos densos e reduzem o volume de GFAP. Houve marcação positiva para o anticorpo anti-S100 em oito ovinos, incluindo os dois ovinos experimentais o que sugere reatividade celular, com proliferação mitocondrial e de retículo endoplasmático liso. Estas alterações são caraterísticas dos efeitos da amônia nos astrócitos. Conclui-se que na intoxicação por T. cinerea em alguns ovinos ocorrem sinais nervosos em consequência da encefalopatia hepática.(AU)

In the semiarid region of northeastern Brazil, Tephrosia cinerea causes periacinar hepatic fibrosis in sheep with severe ascites and, occasionally, nervous signs. Sixteen sheep from six outbreaks of T. cinerea poisoning were studied. All sheep had histologic lesion of periacinar fibrosis and six showed, in the brain, vacuolization (spongy degeneration) of the white matter and junction between grey and white matter and presence of Alzheimer type II astrocytes in the grey matter. The disease was produced experimentally in two sheep, that presented porto-sistemic shunts and similar histologic lesions as those observed in the spontaneous cases. Immunohistochemistry revealed weak labelling with anti-GFAP antibodies suggesting a degenerative alteration of astrocytes with accumulation of dense bodies and reduction of the GFAP. There was strong labelling with anti-S100 antibodies suggesting cellular reactivity with proliferation of mitochondria and endoplasmatic reticulum. Such alterations are characteristic of the effects caused by ammonia on the astrocytes. It is concluded that in poisoning by T. cinerea nervous signs due to hepatic encephalopathy occur in some sheep.(AU)

Kernicterus in an adult dog

Background: Kernicterus or bilirubin encephalopathy is a condition rarely observed in animal characterized by a yellowish discoloration of the central nervous system. It is a potentially fatal condition due to bilirubin neurotoxic effects caused by the increase of non-conjugated bilirubin pigment, which passes blood brain barrier and has been attributed to an imbalance between albumin and bilirubin levels. Intracellular bilirubin is toxic for cells and can cause decrease in protein synthesis, specially albumin, depression of cell respiration and cellular death. This paper describes kernicterus in a 2-year-old Great Dane female dog.Case: Clinically, the animal showed apathy, lethargy, weight loss and jaundice, which progressed to vomiting and neurological signs characterized by loss of consciousness and eventually coma. Blood parameters were within normal range, except for high levels of alanine aminotransferase (523 U/L), suggesting a liver lesion. The animal was submitted to euthanasia due to the poor prognosis, and at post-mortem examination it showed dehydration and severe jaundice, especially oral, vaginal and ocular mucosas, subcutaneous tissue and blood vessels intima surface. The liver had an accentuated lobular pattern, and the stomach mucosa was reddened. Multiple petechiae were observed in the epicardium, as well as icterus in the blood vessels of the heart. Furthermore, the brain and cerebellum cortex, thalamic region and nuclei region of brainstem showed extensive icteric areas. Microscopically, the liver presented a mononuclear portal hepatitis, centrilobular necrosis and presence of yellowish pigments. The brain had neuronal necrosis, mild vacuolization of the white matter, perineuronal edema and Alzheimer type II astrocytes, while cerebellum showed Purkinje cells necrosis. Hepatic cooper measurement was within range values, and direct imunofluorescence for the detection of Leptospira sp. was negative.[...]