Pathophysiology of Portal Hypertension

Iwakiri, Yasuko; Groszmann, Roberto J.

doi:10.1002/9781119436812.ch51

Cited by 16 publications

(19 citation statements)

References 144 publications

(39 reference statements)

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“…Among the existing managements of variceal hemorrhage, splenectomy may be the most promising one. The blood flow is increased in the superior mesenteric arteries and splenic arteries of patients with cirrhosis and portal hypertension, which in turn increases the portal blood flow, exclusively in patients with splenomegaly [17] . PHT, partly due to increased portal blood flow, is responsible for the severe and often lethal complications of cirrhosis, such as bleeding esophageal varices, ascites, renal dysfunction and hepatic encephalopathy.…”

Section: Discussionmentioning

confidence: 99%

Potential Value of Splenectomy for the Life Quality and Long-term Survival of Patients with Cirrhosis

Guo¹,

Gao²,

Xing³

et al. 2020

PAR

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Patients with cirrhosis will gradually develop portal hypertension (PHT) and esophagogastric varices, and subsequently the more severe and often lethal complications such as bleeding esophageal varices, ascites, spontaneous bacterial peritonitis, renal dysfunction and hepatic encephalopathy. To date, there is still not any effective therapy for the prevention of the development these serious complications. The initial factor leading to PHT is an increase in hepatic resistance. Then, the increase in portal blood ?ow contributes to the maintenance and exacerbation of PHT, as well as the formation of esophagogastric varices and lethal complications. Increasing evidence shows that, enlarged spleen not only contributes to the increase in portal venous inflow, but also plays a contributory role in promoting almost all lethal complications of cirrhosis through its resulted hypersplenism together with other mechanisms. So, we hypothesize that prophylactic splenectomy may efficiently delay the progression of cirrhosis and improve life quality and long-term survival of patients with cirrhosis.

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Section: Discussionmentioning

confidence: 99%

Potential Value of Splenectomy for the Life Quality and Long-term Survival of Patients with Cirrhosis

Guo¹,

Gao²,

Xing³

et al. 2020

PAR

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“…Splanchnic and systemic arterial vasodilatations increase the blood flow into the portal venous system (hyperdynamic state) and lead to portal hypertension and collateral formation. [3][4][5][6][7] The hyperdynamic state, especially around the spleen, is detected in patients with portal hypertension. The percentage of splenic venous flow in portal venous flow is approximately 20%-40% in normal liver, approximately 50% in chronic hepatitis and liver cirrhosis, and approximately 75% in idiopathic portal hypertension.…”

Section: Hemodynamics Of Portal Hypertensionmentioning

confidence: 99%

Management of portal hypertension based on portal hemodynamics

Yoshida

Shimizu

Yoshioka

et al. 2021

Hepatology Research

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Portal hypertension is most commonly caused by chronic liver disease. As liver damage progresses, portal pressure gradually elevates and hemodynamics of the portal system gradually change. In normal liver, venous returns from visceral organs join the portal trunk and flow into the liver (hepatopetal blood flow). As portal pressure increases due to liver damage, congestion of some veins of the visceral organ occurs (blood flow to and from). Finally, the direction of some veins (the left gastric vein in particular) of the visceral organ change (hepatofugal blood flow) and develop as collateral veins (portosystemic shunt) to reduce portal pressure. Therefore, esophagogastric varices serve as drainage veins for the portal venous system to reduce the portal pressure. In chronic liver disease, as intrahepatic vascular resistance is increased (backward flow theory) and collateral veins develop, adequate portal hypertension is required to maintain portal flow into the liver through an increase of blood flow into the portal venous system (forward flow theory). Splanchnic and systemic arterial vasodilatations increase the blood flow into the portal venous system (hyperdynamic state) and lead to portal hypertension and collateral formation. Hyperdynamic state, especially around the spleen, is detected in patients with portal hypertension. The spleen is a regulatory organ that maintains portal flow into the liver. In this review, surgical treatment, interventional radiology, endoscopic treatment, and pharmacotherapy for portal hypertension (esophagogastric varices in particular) are described based on the portal hemodynamics using schema.

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“…Varices are a well-known and studied consequence of portal hypertension, 1 leading to frequent hospitalisation of patients every year. 2 Patients with chronic liver cirrhosis typically have portal hypertension and form varices at the rate of 5% per year. 3 Varices are predominantly seen in the gastrointestinal tract, especially the gastro-oesophageal junction.…”

Section: Introductionmentioning

confidence: 99%

The potential lethality of caput medusae

Russo¹,

Bolcato

Aprile

2021

Med Sci Law

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While gastro-oesophageal varices commonly complicate portal hypertension and may be a life-threatening condition, fatal haemorrhaging from cirrhosis-related caput medusae has seldom been described in the scientific literature. This article documents a rare death due to the rupture of a varix in the umbilical area. This case raises a number of points for medico-legal discussion, such as the negative consequences of an erroneous cause of death in evaluating medical malpractice cases and the importance of a thorough external examination of the body in order to ensure this type of vascular lesion is not overlooked.

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Pathophysiology of Portal Hypertension

Cited by 16 publications

References 144 publications

Potential Value of Splenectomy for the Life Quality and Long-term Survival of Patients with Cirrhosis

Potential Value of Splenectomy for the Life Quality and Long-term Survival of Patients with Cirrhosis

Management of portal hypertension based on portal hemodynamics

The potential lethality of caput medusae

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