Grevel V, Schmidt S, Lettow E, Suter P F, Schmidt G U
Tierarztl Prax. 1987;15(2):185-94.
An overview of the circulation of the liver and of the pathogenesis of hepatic encephalopathy as a result of portal vascular anomalies is given. Clinical signs associated with portal systemic shunts are described on the basis of 16 cases, 14 dogs and 2 cats. These animals ranged in age at the time of presentation from 4 months to 7 years. The predominant abnormality observed were central nervous signs, which differed in severity. The different techniques of contrast angiography allowing demonstration of a portal systemic shunt are presented along with a discussion of the pros and cons of each. Additionally the significance of making portal venous pressure measurements prior to each angiography is also explained. In most cases mesenteric portography was chosen. Based on their location the anomalies could be categorized as intrahepatic (4 dogs) or extrahepatic (10 dogs, 2 cats). In both groups breeds of various size are represented. The extrahepatic shunts could be further described as portal-caval (n = 5), portal-phrenic (n = 4) and portal-azygos (n = 3). In five of the older animals angiography showed in addition some hepatic perfusion by the portal vein. Laboratory evaluation revealed increased resting blood ammonia concentrations (greater than 200-912 micrograms/100 ml) in all animals. Seven dogs had definitely subnormal BUN concentrations (less than 10 mg%) and ten dogs low total plasma protein levels (less than 5.4 g%). Free amino acids (24) were determined in four dogs and a lowered hepatic encephalopathy index (less than 1.64) found. Medical palliative therapy to control the clinical signs is discussed. The only effective long term therapy is, however, surgery. The shunt vessel is narrowed so that a greater volume of portal blood reaches the liver. Experience gained from the surgical therapy of 14 animals is presented. Ten of these survived well without requiring further therapy at a later time. Finally the etiology, prognosis, and differential diagnosis are summarized.
本文概述了肝脏的血液循环以及门静脉血管异常导致肝性脑病的发病机制。基于16例病例（14只犬和2只猫）描述了与门体分流相关的临床体征。这些动物就诊时的年龄在4个月至7岁之间。观察到的主要异常是中枢神经体征，其严重程度各不相同。介绍了用于显示门体分流的不同造影技术，并讨论了每种技术的优缺点。此外，还解释了在每次血管造影前测量门静脉压力的意义。在大多数情况下选择肠系膜门静脉造影。根据其位置，这些异常可分为肝内型（4只犬）或肝外型（10只犬，2只猫）。两组中均有不同体型的品种。肝外分流可进一步描述为门静脉 - 腔静脉分流（n = 5）、门静脉 - 膈静脉分流（n = 4）和门静脉 - 奇静脉分流（n = 3）。在5只年龄较大的动物中，血管造影还显示门静脉有一些肝灌注。实验室评估显示所有动物静息血氨浓度升高（大于200 - 912微克/100毫升）。7只犬的尿素氮浓度明显低于正常（小于10毫克%），10只犬的血浆总蛋白水平较低（小于5.4克%）。对4只犬测定了游离氨基酸（24种），发现肝性脑病指数降低（小于1.64）。讨论了控制临床体征的药物姑息治疗。然而，唯一有效的长期治疗方法是手术。使分流血管变窄，以便更多的门静脉血到达肝脏。介绍了14只动物手术治疗的经验。其中10只存活良好，后期无需进一步治疗。最后总结了病因、预后和鉴别诊断。
