19 hours ago Jun 04, 2021 · Portal hypertension is the driver of complications in cirrhosis, such as ascites and gastro-oesophageal varices (which can haemorrhage), as well as hepatic encephalopathy due to portosystemic shunting, hepatorenal syndrome and hypersplenism.5 Patients with complications of portal hypertension show repeating readmissions in the hospital and are described as … >> Go To The Portal
Jun 04, 2021 · Portal hypertension is the driver of complications in cirrhosis, such as ascites and gastro-oesophageal varices (which can haemorrhage), as well as hepatic encephalopathy due to portosystemic shunting, hepatorenal syndrome and hypersplenism.5 Patients with complications of portal hypertension show repeating readmissions in the hospital and are described as …
Mar 10, 2021 · Explanation: Development of portal hypertension is related to the obstruction to portal blood flow which causes an increase in portal venous pressure resulting in splenomegaly, ascites, and collateral venous channels; para-umbilical and hemorrhoidal veins, cardia of the stomach and into the esophagus.
Jul 02, 2019 · The primary pathophysiology stems from portal hypertension, which is induced from an increased resistance to flow secondary to distorted sinusoidal architecture and is further sustained from an increase in portal venous flow. 1 Portal hypertension induces both progressive splanchnic and systemic vasodilation mediated via nitric oxide and other vasoactive molecules …
Feb 07, 2006 · A few cases have been reported where patients with cirrhosis with renal involvement may develop arterial hypertension, especially in patients with early cirrhosis. After the onset of severe cirrhosis most patients with renal hypertension become normotensive, like patients with essential hypertension (Figure (Figure2). 2). However, nephropathy in cirrhosis …
Portal hypertension is a leading side effect of cirrhosis. Your body carries blood to your liver through a large blood vessel called the portal vein. Cirrhosis slows your blood flow and puts stress on the portal vein. This causes high blood pressure known as portal hypertension.Jan 3, 2020
The most common cause of portal hypertension is cirrhosis, or scarring of the liver. Cirrhosis results from the healing of a liver injury caused by hepatitis, alcohol abuse or other causes of liver damage. In cirrhosis, the scar tissue blocks the flow of blood through the liver and slows its processing functions.Nov 16, 2017
The clinical manifestations of portal hypertension may include caput medusae, splenomegaly, edema of the legs, and gynecomastia (less commonly) (Figure 2). Caput medusae is a network of dilated veins surrounding the umbilicus.
An increase in splanchnic blood flow in portal hypertension is the result of a marked vasodilation of arterioles in splanchnic organs, which drain blood into the portal venous system[35].
Variceal hemorrhage is the most common complication associated with portal hypertension. Almost 90% of patients with cirrhosis develop varices, and approximately 30% of varices bleed.Nov 30, 2017
Portal hypertension is elevated pressure in your portal venous system. The portal vein is a major vein that leads to the liver. The most common cause of portal hypertension is cirrhosis (scarring) of the liver.
With regard to the liver itself, causes of portal hypertension usually are classified as prehepatic, intrahepatic, and posthepatic.Nov 30, 2017
The portal venous pressure can be measured directly using either a transjugular approach to the portal vein via the hepatic veins, or by direct puncture of the portal vein through a percutaneous transhepatic route under ultrasound guidance. A catheter is then passed over a guidewire into the main portal vein.
To evaluate the accuracy of spleen stiffness (SS) and liver stiffness (LS) measured by using acoustic radiation force impulse imaging in the diagnosis of portal hypertension in patients with liver cirrhosis, with the hepatic venous pressure gradient (HVPG) as a reference standard.
Institutional review board approval and informed consent were obtained for this prospective single-center study.
The correlation coefficient between SS and HVPG ( r = 0.876) was significantly better than that between LS and HVPG ( r = 0.609, P < .0001).
SS is reliable and has better diagnostic performance than LS for identifying portal hypertension in liver cirrhosis.
The development of portal hypertension is a common consequence of chronic liver diseases and leads to the major complications of liver cirrhosis, such as ascites, hepatic encephalopathy, variceal bleeding, and decompensation.
This study was performed in accordance with the guidelines of and was approved by our institutional review board. Written informed consent was obtained.
Among the 62 patients who satisfied the inclusion criteria, two had an inconclusive SS measurement because the spleen was poorly visualized secondary to obesity or gastrointestinal gas. In total, there were 60 patients in the final analysis group.
The reason is that due to the above-mentioned changes and mechanisms, there is a perpetuation of injury guaranteeing the progression and worsening of prognosis in liver cirrhosis.
Portal hypertension is defined as increased pressure within the portal vein, which is the blood vessel connecting the outflow of the gastro-intestine and spleen (splanchnic organs) and the liver.
HRS is the maximal form of kidney dysfunction in cirrhosis and is basically a functional failure due to intrarenal vascoconstriction, but also at least partly induced by the decreased effective arterial blood volume, following long-standing portal hypertension and hyperdynamic circulation ( 166 ).
HSC is the hepatic pericyte involved in the vessel formation and stabilization ( 43 ). In this role, HSCs follow the transformation of LSEC upon injury (see above) and also drive LSEC transformation by release of VEGF, which works in a paracrine and autocrine manner on LSECs and HSCs ( 43 ). Especially, platelet-derived growth factor (PDGF) is an important factor, which not only recruits HSCs in their pericyte function, but also by boosting fibrogenic potential in these cells. The boost in hepatic angiogenesis is probably meant to be a repair mechanism, but it aggravates the liver pathology and does not alleviate portal hypertension ( 43, 44 ). The reason is that these newly formed vessels are different from the sinusoidal vasculature, and do not increase the blood perfusion of the cirrhotic liver, but they further impair the homeostasis of hepatocytes and aggravate liver damage, further fuel fibrosis and inflammation ( 45 ). In experimental work several anti-angiogenic strategies have shown to be beneficial for portal hypertension, which at least was in part due to improved fibrosis ( 46, 47, 48, 49 ). Further targets to be addressed maybe Vasohibin-1 ( 50) and placental growth factor (PlGF) ( 51 ). But in these studies, the effect on portal hypertension was at least partially due to the anti-angiogenic effect on the extrahepatic angiogenesis. Since the hepatic resistance is at least partly dependent on the fibrosis, it is difficult, or even impossible to separate the role of intrahepatic angiogenesis on portal hypertension from the role on fibrosis. Along the transdifferentiation of HSC, the fibrogenic and angiogenic potential increases with the development of a myofibroblastic apparatus enabling contraction. Contraction is the dynamic part of hepatic resistance.
LSECs have fenestrae of approximately 0.1 microns organized into groups of sieve plates, which facilita te the transport of macromolecules from the hepatic sinusoids to the space of Disse, then to HSCs and hepatocytes. Additionally, a unique feature of LSECs distinguishing them from endothelial cells in other organs is the lack of a basement membrane, which allows efficient movement of macromolecules between the lumen of the sinusoid and the space of Disse ( 7 ). Loss of fenestrae and appearance of a basement membrane in LSECs is termed “capillarization” ( 8, 9 ). Vascular endothelial growth factor (VEGF) has been known as a key factor that maintains the fenestrae without basement membrane ( 10) through endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) signaling ( 11 ). A study showed that removal of VEGF signaling in transgenic mice, in which liver-specific secretion of a soluble VEGF decoy receptor inactivates endogenous VEGF, results in a loss of LSEC fenestration and portal hypertension as well as HSC activation independent of hepatic parenchymal damage. Administration of VEGF to these mice ameliorated portal hypertension ( 12 ). In addition, the composition of collagen in the space of Disse may play a role in maintenance or a loss of endothelial fenestration ( 13 ). A recent study in mice showed that Dll4, a ligand of the Notch signaling pathway with a predominant expression in endothelial cells (ECs) promotes LSEC capillarization by basement membrane formation ( 14 ). Additionally, this study showed that Dll4 knockdown in human LSEC cell line decreased extracellular matrix (ECM) expression while its overexpression showed an increase in ECM proteins including collagens, fibronectin and laminin, confirming the role of Dll4 in LSEC capillarization (14).
Hepatic cells. Among the hepatic cells involved in the development of portal hypertension, LSECs and HSCs are directly involved in the increased hepatic resistance. Thus, their modulation may on the one side relieve the pressure and on the other side improve on the longer run liver fibrosis.
Therefore, the treatment of complications of portal hypertension by NSBB may have narrow windows of opportunity ( 163 ). Generally speaking, NSBB is for acute events rather contraindicated, since the required portal venous decompression needs to be achieved fast at a large magnitude.