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A 1-year-old mixed breed dog initially presented with marked ascites due to a low-protein transudate resulting from portal hypertension. Laboratory evaluation revealed non-regenerative anemia, lymphopenia, thrombocytopenia, evidence of hepatic insufficiency [hypoalbuminemia, decreased urea, increased post-prandial bile acids, prolonged activated partial thromboplastin time (aPTT)] and Ehrlichia canis infection. Approximately a week later, the dog was declining and was euthanized. On autopsy, multifocal hepatic granulomas and acquired portosystemic shunts (APSS) were seen. Imprint cytology revealed fungal hyphae and pyogranulomatous inflammation in the liver and brain. Disseminated Cladophialophora bantiana phaeohyphomycosis was diagnosed by histologic examination, culture and PCR. Immunosuppression due to ehrlichiosis is suspected to have predisposed this animal to fungal infection. To the authors' knowledge, this is the first report of C. bantiana in the West Indies.

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Portal vein thrombosis is a rare complication after laparoscopic sleeve gastrectomy, a widely performed bariatric surgery procedure. Occasionally, the development of portal vein thrombosis can progress to more severe conditions, including portal hypertension and cavernomatosis, thereby presenting a complex and challenging clinical scenario. The management of such complications often requires careful consideration; however, surgical intervention in the form of a splenorenal shunt is an exceptional indication. We present the case of a 33-year-old female patient who had previously undergone laparoscopic sleeve gastrectomy in 2014 and subsequently developed portal thrombosis, followed by cavernomatosis and associated complications of portal hypertension. A proximal splenorenal shunt procedure and splenectomy were successfully performed to manage portal hypertension. The presentation of this clinical case aims to contribute to the available evidence and knowledge surrounding this rare and challenging pathology.

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En los últimos años, la trombosis de la vena porta entre los pacientes cirróticos se ha comportado como una entidad reconocida y cada vez más estudiada, no solo por su creciente incidencia, sino por la asociación con gravedad y mal pronóstico en cirrosis. Asimismo, se hacen objeto de estudio las terapias disponibles para el manejo tanto médico como quirúrgico de estos pacientes, lo que ha dado un papel importante a la derivación portosistémica transyugular intrahepática (TIPS). El uso de TIPS en esta población se posiciona como una alternativa de manejo aceptable, no solo por brindar mejoría en las complicaciones derivadas de la hipertensión portal, sino también por sus resultados prometedores en diferentes estudios sobre el flujo y la recanalización portal, y por su perfil de seguridad. Sin embargo, la eficacia, los efectos adversos a largo plazo y el pronóstico de dicha intervención en la compleja fisiopatología de la cirrosis deben continuar en estudio. El objetivo de este artículo es revisar los avances del uso de TIPS en el manejo de pacientes con cirrosis hepática y trombosis portal.

In recent years, portal vein thrombosis among cirrhotic patients has been a well-recognized and continuously studied entity, not only because of its increasing incidence but also because of its association with severity and poor prognosis in cirrhosis. Likewise, therapies available for both medical and surgical management in these patients are being studied, which has given an important role to the transjugular intrahepatic portosystemic shunt (TIPS). The use of TIPS in this population is positioned as an acceptable management alternative, not only because it provides improvement in complications derived from portal hypertension, but also because of its promising results in different studies on portal flow and recanalization upgrade, and for its safety. However, the efficacy, long-term adverse effects, and prognosis of this intervention in the complex pathophysiology of cirrhosis must continue to be studied. The objective of this article is to review the advances in the use of TIPS in the management of patients with liver cirrhosis and portal vein thrombosis.

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El shunt portosistémico congénito es una anomalía vascular venosa que comunica circulación portal y sistémica, por la que se deriva el flujo sanguíneo, salteando el paso hepático. Es una entidad poco frecuente, cuya incidencia varía entre 1/30 000 y 1/50 000 recién nacidos. Puede cursar de forma asintomática o presentarse con complicaciones en la edad pediátrica o, menos frecuente, en la edad neonatal. Ante el diagnóstico, se deberá definir la necesidad de intervención quirúrgica o intravascular para el cierre. Esta decisión depende de las características anatómicas de la malformación, de las manifestaciones clínicas y complicaciones presentes. Se presenta el caso de un paciente de un mes de vida derivado a nuestro centro para estudio de hepatitis colestásica neonatal, con diagnóstico de shunt portosistémico extrahepático. Se realizó cierre intravascular de la lesión con mejoría significativa posterior.

Congenital portosystemic shunt is a venous vascular abnormality that connects portal and systemic circulation, resulting in diversion of the blood flow, bypassing the hepatic passage. It is a rare malformation; its incidence varies from 1:30 000 to 1:50 000 newborns. It may be asymptomatic or present with complications in the pediatric age or, less frequently, in the neonatal age. Upon diagnosis, the need for a surgical or an intravascular intervention for closure should be defined. This decision depends on the malformation anatomical characteristics, clinical manifestations, and complications. We present the case of a 1-month-old patient referred to our center for the study of neonatal cholestatic hepatitis, with a diagnosis of extrahepatic portosystemic shunt. Intravascular closure of the defect was performed with significant subsequent improvement.

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Congenital portosystemic shunt is a venous vascular abnormality that connects portal and systemic circulation, resulting in diversion of the blood flow, bypassing the hepatic passage. It is a rare malformation; its incidence varies from 1:30 000 to 1:50 000 newborns. It may be asymptomatic or present with complications in the pediatric age or, less frequently, in the neonatal age. Upon diagnosis, the need for a surgical or an intravascular intervention for closure should be defined. This decision depends on the malformation anatomical characteristics, clinical manifestations, and complications. We present the case of a 1-month-old patient referred to our center for the study of neonatal cholestatic hepatitis, with a diagnosis of extrahepatic portosystemic shunt. Intravascular closure of the defect was performed with significant subsequent improvement.

El shunt portosistémico congénito es una anomalía vascular venosa que comunica circulación portal y sistémica, por la que se deriva el flujo sanguíneo, salteando el paso hepático. Es una entidad poco frecuente, cuya incidencia varía entre 1/30 000 y 1/50 000 recién nacidos. Puede cursar de forma asintomática o presentarse con complicaciones en la edad pediátrica o, menos frecuente, en la edad neonatal. Ante el diagnóstico, se deberá definir la necesidad de intervención quirúrgica o intravascular para el cierre. Esta decisión depende de las características anatómicas de la malformación, de las manifestaciones clínicas y complicaciones presentes. Se presenta el caso de un paciente de un mes de vida derivado a nuestro centro para estudio de hepatitis colestásica neonatal, con diagnóstico de shunt portosistémico extrahepático. Se realizó cierre intravascular de la lesión con mejoría significativa posterior.

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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.

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La hipertensión portal es una de las principales complicaciones de la cirrosis. El papel de la derivación portosistémica transyugular intrahepática (TIPS, por sus siglas en inglés), ha ganado aceptación como tratamiento efectivo en la hipertensión portal. En los últimos años su técnica se ha ido perfeccionando, disminuyendo la morbimortalidad relacionada con este procedimiento. Describimos un caso de un paciente masculino con cirrosis Child-Pugh 8 y MELD 16, con antecedente de descompensación por sangrado variceal recurrente y trombosis parcial de la vena porta, con un gradiente de presión venosa hepática (GPVH) de 20 mmHg, por lo que es llevado a TIPS como profilaxis secundaria, con un gradiente final post-TIPS de 6 mmHg. Posterior al procedimiento, presentó evolución tórpida con deterioro de las pruebas de bioquímica hepática. Se realizó una angiografía demostrando permeabilidad del TIPS sin progresión de la trombosis portal, y hallazgos anormales inespecíficos de la arteria hepática. Se decidió realizar una arteriografía selectiva, demostrando un pseudoaneurisma de la rama derecha de la arteria hepática y una fístula arteriovenosa de la arteria hepática a las colaterales portales. Se realizó embolización selectiva de la fístula con evolución satisfactoria del paciente.

Portal hypertension is a life-threatening complication of cirrhosis. The role of transyugular intrahepatic portosystemic shunt (TIPS) has gained acceptance as an effective treatment for portal hypertension. In the past few years, its technique has been improved, decreasing the mortality related with the procedure. We describe a case of a male with Child-Pugh 8 and MELD 16 cirrhosis, with previous decompensation of recurrent variceal bleeding and partial thrombosis of the portal vein. TIPS was performed due to a hepatic venous pressure gradient (HVPG) of 20 mmHg. The final measure showed HVPG of 6 mmHg. After the procedure, he presented a torpid evolution with deterioration of liver function tests. An angiography was performed demonstrating patency of the TIPS without progression of portal thrombosis and nonspecific abnormal findings of the hepatic artery. Selective arteriography was performed and revealed a pseudoaneurysm of the right branch of the hepatic artery and an arteriovenous fistula (AVF) from the hepatic artery to portal collaterals. Embolization was performed to treat the fistula with satisfactory evolution of the patient.

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La obstrucción en el tracto de salida del flujo venoso hepático, también conocida como síndrome de Budd-Chiari, es una condición infrecuente que causa congestión hepática, hipertensión portal, ne-crosis de los hepatocitos y, eventualmente, falla hepática aguda o crónica. Actualmente, el manejo de esta condición representa un reto para el médico, quien debe estar preparado para determinar la mejor alternativa entre las diferentes opciones terapéuticas disponibles. Este artículo pretende ilus-trar las alternativas del manejo intervencionista de esta enfermedad, a través de una serie de casos de pacientes tratados en el servicio de Radiología Intervencionista de un hospital de referencia de la ciudad de Medellín, entre 2011 y 2017.

Hepatic venous outflow tract obstruction, also known as Budd-Chiari syndrome, is a rare condition that causes hepatic congestion, portal hypertension, hepatocyte necrosis and eventually acute or chronic liver failure. Currently, the management of this condition represents a challenge for the physi-cian, who must be prepared to determine the best alternative among the different therapeutic options available. This article aims to illustrate the alternatives of interventional management of this disease, through a series of cases of patients treated in the Interventional Radiology service of a referral hos-pital in the city of Medellin, between 2011 and 2017.

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INTRODUCTION AND AIMS: Orthotopic liver transplant (OLT) is the definitive treatment of most types of liver failure. Transjugular intrahepatic portosystemic shunt (TIPS) and portocaval shunt placement procedures reduce the systemic vascular complications of portal hypertension. TIPS placement remains a "bridge" therapy that enables treatment of refractory symptoms until transplantation becomes available. The aim of the present study was to describe the operative impact of TIPS prior to OLT. MATERIALS AND METHODS: A retrospective review was conducted on patients that underwent liver transplant at the Hospital San José within the timeframe of 1999 and February 2020. RESULTS: We reviewed a total of 92 patients with OLT. Sixty-six patients were male and 26 were female, with a mean age of 52 years. Nine (9.8%) of the 92 patients had a TIPS, before the OLT. Preoperative Child-Pugh class, MELD score, and sodium and platelet levels were similar between groups. We found no difference in the means of intensive care unit stay, operative time, or blood transfusions for liver transplant, with or without previous TIPS. There was no significant difference between groups regarding vascular and biliary complication rates or the need for early intervention. The overall one-year mortality rate in the TIPS group was 11%. CONCLUSIONS: TIPS is an appropriate therapeutic bridge towards liver transplant. We found no greater operative or postoperative complications in patients with TIPS before OLT, when compared with OLT patients without TIPS. The need for transfusion, operative time, and ICU stay were similar in both groups.

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BACKGROUND: Hepatic encephalopathy (HE) is a common complication of cirrhosis associated with a reduced survival. The presence of high-flux spontaneous porto-systemic shunts can induce HE even in patients with preserved liver function. AIM: To evaluate the effect of spontaneous porto-systemic shunt embolization (SPSE) over HE and its long-term evolution. MATERIAL AND METHODS: Retrospective analysis of 11 patients (91% males) with severe HE non-responsive to medical treatment in whom a SPSE was performed. The grade of HE (employing West Haven score), survival, MELD and Child-Pugh score, ammonia levels, degree of disability (employing the modified Rankin scale (mRs)) were evaluated before and at thirty days after procedure. RESULTS: The most common etiology found was non-alcoholic steatohepatitis (63.6%). A reduction of at least two score points of HE was observed in all patients after thirty days. There was a significant reduction on median (IQR) West Haven score from 3 (2-3) at baseline to 1 (0-1) after the procedure (p < 0.01). Twelve months survival was 63.6%. There was a decrease in median ammonia level from 106.5 (79-165) (ug/dL) to 56 (43-61) after SPSE (p = 0.006). The median mRS score before and after the procedure was 3 (3-5) and 1 (1-2.5), respectively (p < 0.01). Conclusions: According to our experience, SPSE is a feasible and effective alternative to improve HE and functionality of patients with refractory EH.

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PURPOSE: To evaluate liver function improvement and volume gain after percutaneous recanalization of chronic portal vein thrombosis (PVT) in non-cirrhotic patients. MATERIALS AND METHODS: In this retrospective study, five non-cirrhotic participants between 21 and 67 years old with secondary chronic PVT (4-21 years from diagnose) were submitted to percutaneous portal vein recanalization, followed by varices and shunts embolization. RESULTS: After a mean of 12.6 months, all portal veins remained patent and there was complete resolution of portal hypertension (PH) symptoms in all participants. There was a significant increase in liver volume of 39.8 ± 19.0% (p = 0.042), platelets count of 53120 ± 20188/µl (p = 0.042), and a significant decrease in total bilirubin levels from 1.04 ± 0.23 mg/dL to 0.51 ± 0.09 mg/dL (p = 0.043). We also found a non-significant increase in albumin levels from 3.88 ± 0.39 g/dL to 4.38 ± 0.27 g/dL (p = 0.078) and decrease in spleen diameter from 16.88 ± 4.03 cm to 14.15 ± 2.72 cm (p = 0.068). DISCUSSION: In this retrospective study, even with a small number of participants, we were capable of showing a median of 39.8% increase in liver volume, laboratorial liver function improvement, platelets count and resolution of PH symptoms, including gastroesophageal varices disappearance after portal vein recanalization followed by shunt embolization. CONCLUSION: In this small series of cases, recanalization of chronic PVT in non-cirrhotic participants was feasible, successful and safe despite the prolonged time of occlusion. This is a new and promising approaching to an old and still challenging disease.

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A 39-year-old female, liver transplanted for Autosomic Dominant Polycystic Kidney Disease (ADPKD) developed refractory ascites early after surgery, with frequent need of large-volume paracentesis. This was associated with severe sarcopenia and kidney impairment. Liver biopsy showed a sinusoidal congestion with a significant enlargement of hepatic portal veins. This picture suggested the diagnosis of vascular obstructions. Due to an unfavorable passage through the piggy-back surgical anastomosis and the angle between the hepatic veins and the portal branches, a conventional placement of a transjugular portosystemic shunt (TIPS) was not feasible. An alternative approach was pursued with success, using a combined percutaneous-transjugular approach and achieving a complete recovery of ascites, sarcopenia and renal function.

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La trombosis de la vena porta (TVP) se define como una oclusión parcial o completa de la luz de la vena porta o sus afluentes por la formación de trombos. La etiología de la formación de TVP en un hígado cirrótico parece ser multifactorial, y presenta una prevalencia de 1,3% a 9,8%. La fisiopatología de la TVP en pacientes con cirrosis aún no se comprende completamente, pero se sabe que existe una disminución de la síntesis tanto de factores procoagulantes como de anticoagulantes, que asociados a factores de riesgo locales o sistémicos, favorecen el predominio de los procoagulantes que causan la trombosis. Establecer el momento de la instauración de la trombosis y el nivel anatómico dentro del sistema venoso espleno-mesentérico, son aspectos fundamentales para estimar el pronóstico y ayudar a la toma de decisiones terapéuticas. A pesar de que hasta la fecha no se ha publicado un consenso sobre su profilaxis o tratamiento en la cirrosis hepática, y existen muchas controversias con respecto al manejo óptimo de la TVP, se han observado beneficios generales de la anticoagulación con heparina de bajo peso molecular en pacientes con cirrosis hepática, en particular en aquellos con TVP aguda. El objetivo de esta revisión es explorar los temas más relevantes al momento de abordar un paciente con cirrosis hepática y TVP.

Portal vein thrombosis (PVT) is defined as a partial or complete occlusion of the lumen of the portal vein or its tributaries due to the formation of thrombi. The etiology of DVT formation in a cirrhotic liver appears to be multifactorial, with a prevalence of 1.3% to 9.8%. The pathophysiology of PVT in patients with cirrhosis is not yet fully understood, but it is known that there is a decrease in the synthesis of both procoagulant and anticoagulant factors, which associated with local or systemic risk factors, favor the predominance of procoagulants that cause thrombosis. Establishing the onset of thrombosis and the anatomical level within the splanchnic mesenteric venous system are fundamental aspects to estimate the prognosis and aid in therapeutic decision-making. Despite the fact that to date no consensus has been published on its prophylaxis or treatment in liver cirrhosis, and the many controversies regarding the optimal management of PVT, general benefits of anticoagulation with low molecular weight heparin have been observed in patients with liver cirrhosis, particularly those with acute PVT. The objective of this review is to explore the most relevant issues when approaching a patient with liver cirrhosis and PVT.

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Congenital portosystemic shunt (CPSS) is a rare disorder characterized by a diversion of Porto-mesenteric blood into systemic veins. Type I is an end to side fistula between the portal vein and the inferior vena cava. Type II is a side to side fistula between the main portal vein or its branches and mesenteric, splenic, gastric, and systemic veins. Clinical presentation of these patients varies. Treatment and management are guided by the type of malformation and clinical presentation. Herein, we present a case of CPSS Type IIb with neurological symptoms, treated with endovascular occlusion with 6-year follow-up without remission.

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El síndrome de Budd-Chiari (SBC), descrito en 1845, se define como la obstrucción del flujo venoso hepático en ausencia de enfermedad cardíaca o pericárdica. En Colombia no se tienen datos epidemiológicos claros de esta patología, la cual alrededor del mundo se considera poco frecuente. Se diagnostica al demostrar la obstrucción del flujo de las venas hepáticas. Tiene diversas manifestaciones clínicas como fiebre, ascitis, dolor abdominal y circulación colateral, entre otras. En ciertos casos es asintomática y en su gran mayoría se acompaña de patologías protrombóticas. El manejo inicial depende de la condición del paciente; sin embargo, se ha propuesto el manejo escalonado, donde se inicia con anticoagulación, se continúa con angioplastia, luego con desvío portosistémico intrahepático transyugular (TIPS), y se termina con trasplante hepático. El pronóstico depende de un diagnóstico precoz y un tratamiento adecuado. En las mejores circunstancias se alcanza una sobrevida a cinco años en el 90% de los casos, mientras que en ausencia de manejo, la tasa de mortalidad a un año alcanza el mismo porcentaje.

Budd-Chiari syndrome (SBC), described in 1845, is defined as the obstruction of hepatic venous flow in the absence of heart or pericardial disease. In Colombia there are no clear epidemiological data of this pathology, that around the world is considered rare. It is diagnosed by demonstrating the obstruction of the flow of the hepatic veins. It has various clinical manifestations such as fever, ascites, abdominal pain and collateral circulation, among others. In certain cases, it is asymptomatic but in the great majority it is accompanied by prothrombotic pathologies. Initial management depends on the patient's condition; however, staggered management has been proposed, beginning with anticoagulation, continuing with angioplasty, then with transjugular intrahepatic portosystemic shunt (TIPS), and finally, with liver transplantation. The prognosis depends on an early diagnosis and proper treatment. In the best circumstances, a five-year survival is achieved in 90% of cases, while in the absence of treatment, the one-year mortality rate reaches the same percentage.

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Parastomal variceal bleeding (PVB) is a serious complication occurring in up to 27% of patients with an ostomy and concurrent cirrhosis and portal hypertension. The management of PVB is difficult and there are no clear guidelines on this matter. Transjugular intrahepatic portosystemic shunt (TIPS), sclerotherapy, and /or coil embolization are all therapies that have been shown to successfully manage PVB. We present a case series with five different patients who had a PVB at our institution. The aim of this case series is to report our experience on the management of this infrequently reported but serious condition. We also conducted a systemic literature review focusing on the treatment modalities of 163 patients with parastomal variceal bleeds. In our series, patient 1 had embolization and sclerotherapy without control of bleed and expired on the day of intervention due to hemorrhagic shock. Patient 2 had TIPS in conjunction with embolization and sclerotherapy and had no instance of rebleed 441 days after therapy. Patient 3 did not undergo any intervention due to high risk for morbidity and mortality, the bleed self-resolved and there was no further rebleed, this same patient died of sepsis 73 days later. Patient 4 had embolization and sclerotherapy and had no instance of rebleed 290 days after therapy. Patient 5 had TIPS procedure and was discharged five days post procedure without rebleed, patient has since been lost to follow-up.

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Background: Portosystemic deviation (PSD) is a congenital or acquired vascular anomaly that allows an abnormal bloodflow from the portal vein directly to the systemic circulation. This liver by-pass avoids hepatic metabolism of severaltoxins. Congenital PSDs are usually solitary and extra-hepatic, with a high incidence in pure-breed dogs. Acquired PSDsare usually multiple and occur as a consequence of portal hypertension. Surgery is the definitive treatment. Cliniciansand surgeons may present difficulties in the propaedeutic of animals with PSD. This paper aims at reporting a successfulsurgical treatment of a solitary extra-hepatic congenital PSD in a mixed-breed dog.Case: A 7-month-old mixed-breed dog, female, spayed, weighing 8 kg, was presented with a history of sudden syncopeafter feeding. Complementary exams revealed normocytic hypochromic anaemia, hypoalbuminemia and increased alanineaminotransferase and alkaline phosphatase. Abdominal ultrasound revealed an anomalous vessel inserted in the caudalcava vein, compatible with a congenital extra-hepatic PSD. Computed tomography revealed the anomalous vessel, with1,1 cm of diameter, originated from the cranial mesenteric vein and it inserted in the cranial margin of the caudal cavavein. A medical support was started with hydration, metronidazole, lactulose, probiotic and Hepatic diet. After 15 days thedog was submitted to surgery and a 5 mm ameroid constrictor ring was placed to gradually close the anomalous vessel.The dog recovered well and an abdominal ultrasound was repeated after 30 days, showing the ameroid constrictor ringring in the left cranial abdominal region, occluding the PSD close to its insertion in the caudal cava vein...

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Background: Portosystemic deviation (PSD) is a congenital or acquired vascular anomaly that allows an abnormal bloodflow from the portal vein directly to the systemic circulation. This liver by-pass avoids hepatic metabolism of severaltoxins. Congenital PSDs are usually solitary and extra-hepatic, with a high incidence in pure-breed dogs. Acquired PSDsare usually multiple and occur as a consequence of portal hypertension. Surgery is the definitive treatment. Cliniciansand surgeons may present difficulties in the propaedeutic of animals with PSD. This paper aims at reporting a successfulsurgical treatment of a solitary extra-hepatic congenital PSD in a mixed-breed dog.Case: A 7-month-old mixed-breed dog, female, spayed, weighing 8 kg, was presented with a history of sudden syncopeafter feeding. Complementary exams revealed normocytic hypochromic anaemia, hypoalbuminemia and increased alanineaminotransferase and alkaline phosphatase. Abdominal ultrasound revealed an anomalous vessel inserted in the caudalcava vein, compatible with a congenital extra-hepatic PSD. Computed tomography revealed the anomalous vessel, with1,1 cm of diameter, originated from the cranial mesenteric vein and it inserted in the cranial margin of the caudal cavavein. A medical support was started with hydration, metronidazole, lactulose, probiotic and Hepatic diet. After 15 days thedog was submitted to surgery and a 5 mm ameroid constrictor ring was placed to gradually close the anomalous vessel.The dog recovered well and an abdominal ultrasound was repeated after 30 days, showing the ameroid constrictor ringring in the left cranial abdominal region, occluding the PSD close to its insertion in the caudal cava vein...(AU)

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