Portal Hypertension: Pathophysiology, Diagnosis, and Treatment

Abstract

Portal hypertension (PH) is the result of increased vascular resistance in the portal circulation, increased portal venous blood flow, or both. In veterinary medicine, where portal pressure is seldom measured directly, the diagnosis of PH often is inferred from identification of associated complications including multiple acquired portosystemic shunts, ascites, and hepatic encephalopathy. Likewise, treatment of PH primarily is aimed at controlling these complications. The goal of this review is to provide an update on the pathophysiology, diagnosis, and treatment of PH. The review draws from information in the veterinary hepatology literature, reviews, and consensus statements in human hepatology and the literature on experimental models of PH.

Three Minimally Invasive Methods of Measuring of Portal Vein Pressure in Healthy Dogs

“…74(10): 1299-1302, 2012 Portal hypertension (PH) is caused by excessive resistance to a given blood flow in the portal circulation, and it is classified based on anatomical localization, such as prehepatic, intrahepatic, and posthepatic. In dogs, intrahepatic PH can be caused by parenchymal liver diseases, such as severe chronic hepatitis/cirrhosis (CH) and primary hypoplasia of the portal vein (PHPV) [3,16]. Although understanding portal vein pressure (PVP) is important to identify whether these conditions involve PH, PH has been indirectly indicated in dogs based on clinical consequences including the development of ascites and acquired portosystemic collaterals (APSCs) [3,16].…”

Unusual haemodynamics in two dogs and two cats with portosystemic shunt - implications for distinguishing between congenital and acquired conditions

“…In veterinary medical literature the classical expected clinical and imaging findings in patients with portal hypertension are ascites, multiple APSS (either varices and large shunts) and a confirmed cause of portal flow obstruction at level of extrahepatic portal vein, liver, hepatic veins, posthepatic caudal vena cava, or right atrium (Buob et al, 2011). http://www.openveterinaryjournal.com M. Ricciardi Open Veterinary Journal, (2017 On the other hand patients with congenital PSS are traditionally described as having a single porto-caval connection without ascites or portal flow obstruction (Szatmari et al, 2004;Bertolini et al, 2006;Nelson and Nelson, 2011;Fukushima et al, 2014).…”

“…7(2): 86-94 ________________________________________________________________________________________________________ 92 Regarding the hypothesis no. 1, NCPH is one of the most reported cause of presinusoidal intrahepatic PH in humans and dogs and, from histopathological point of view, it resembles primary hypoplasia of the portal vasculature (PHPV) so that the latter term is recommended by the World Small Animal Veterinary Association liver study group (Buob et al, 2011). It is unclear, however, if the lesion in NCPH-PHPV patients is in all cases a primary hypoplasia of the intrahepatic portal vasculature or a consequence of a primary congenital or acquired disorder in hepatic perfusion (Buob et al, 2011).…”

“…1, NCPH is one of the most reported cause of presinusoidal intrahepatic PH in humans and dogs and, from histopathological point of view, it resembles primary hypoplasia of the portal vasculature (PHPV) so that the latter term is recommended by the World Small Animal Veterinary Association liver study group (Buob et al, 2011). It is unclear, however, if the lesion in NCPH-PHPV patients is in all cases a primary hypoplasia of the intrahepatic portal vasculature or a consequence of a primary congenital or acquired disorder in hepatic perfusion (Buob et al, 2011). In humans the basic criteria to diagnose NCPH are: 1) presence of unequivocal signs of portal hypertension, 2) absence of diffuse liver diseases that can cause PH and 3) absence of occlusive disorders of the hepatic veins or of the portal vein (Schouten et al, 2015).…”

Efeito da hepatectomia parcial associada à administração de fatores nutricionais hepatotróficos sobre a morfologia, função e expressão de genes pró-fibróticos na cirrose hepática em ratos Wistar induzida por tiocetamida

“…Ela é caracterizada pela fibrose intensa e formação de nódulos regenerativos, que resultam na desorganização da arquitetura lobular e vascular hepática. Esse conjunto de características reduz o contato do sangue com os hepatócitos devido à redução das fenestrações sinusoidais, que pode afetar a disponibilidade de nutrientes e fatores hepatotróficos para os hepatócitos e deteriorar suas funções (Bedossa e Paradis, 2003), bem como aumentar a resistência vascular intra-hepática com consecutivo aumento da pressão portal (Buob et al, 2011). Por consequência, a cirrose foi considerada o estágio final e irreversível das lesões crônicas, mesmo que eliminada a causa subjacente (Horiguchi et al, 2009;Lefton et al, 2009), embora haja alguns estudos clínicos que têm mostrado que a cirrose pode regredir dependendo da etiologia e do sucesso do tratamento desta causa (Kawada, 2011).…”