Portal hypertension

a review of portosystemic collateral pathways and endovascular interventions

A. K. Pillai, B. Andring, A. Patel, C. Trimmer, S. P. Kalva

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

The portal vein is formed at the confluence of the splenic and superior mesenteric vein behind the head of the pancreas. Normal blood pressure within the portal system varies between 5 and 10 mmHg. Portal hypertension is defined when the gradient between the portal and systemic venous blood pressure exceeds 5 mmHg. The most common cause of portal hypertension is cirrhosis. In cirrhosis, portal hypertension develops due to extensive fibrosis within the liver parenchyma causing increased vascular resistance. In addition, the inability of the liver to metabolise certain vasodilators leads to hyperdynamic splanchnic circulation resulting in increased portal blood flow. Decompression of the portal pressure is achieved by formation of portosystemic collaterals. In this review, we will discuss the pathophysiology, anatomy, and imaging findings of spontaneous portosystemic collaterals and clinical manifestations of portal hypertension with emphasis on the role of interventional radiology in the management of complications related to portal hypertension.

Original languageEnglish (US)
Article number4130
Pages (from-to)1047-1059
Number of pages13
JournalClinical Radiology
Volume70
Issue number10
DOIs
StatePublished - Oct 1 2015

Fingerprint

Portal Hypertension
Fibrosis
Splanchnic Circulation
Portal System
Portal Pressure
Mesenteric Veins
Interventional Radiology
Venous Pressure
Portal Vein
Decompression
Vasodilator Agents
Liver Cirrhosis
Vascular Resistance
Pancreas
Anatomy
Blood Pressure
Liver

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging

Cite this

Portal hypertension : a review of portosystemic collateral pathways and endovascular interventions. / Pillai, A. K.; Andring, B.; Patel, A.; Trimmer, C.; Kalva, S. P.

In: Clinical Radiology, Vol. 70, No. 10, 4130, 01.10.2015, p. 1047-1059.

Research output: Contribution to journalArticle

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