Ultrasonography for Noninvasive Assessment of Portal Hypertension

Abstract

Portal hypertension is a major pathophysiology in patients with cirrhosis. Portal pressure is the gold standard to evaluate the severity of portal hypertension, and radiological intervention is the only procedure for pressure measurement. Ultrasound (US) is a simple and noninvasive imaging modality available worldwide. B-mode imaging allows broad applications for patients to detect and characterize chronic liver diseases and focal hepatic lesions. The Doppler technique offers real-time observation of blood flow with qualitative and quantitative assessments, and the application of microbubble-based contrast agents has improved the detectability of peripheral blood flow. In addition, elastography for the liver and spleen covers a wider field beyond the original purpose of fibrosis assessment. These developments enhance the practical use of US in the evaluation of portal hemodynamic abnormalities. This article reviews the recent progress of US in the assessment of portal hypertension.

Abdominal imaging findings in adult patients with Fontan circulation

“…On Doppler US, normal hepatic vein shows a triphasic waveform, consisting of a hepatopetal (coming towards the liver) phase occurring during atrial systole and two hepatofugal phases related to atrial and ventricular diastole. Loss of the hepatopetal phase is typically considered to represent increased stiffness of the liver such as in hepatic fibrosis, steatohepatitis and cirrhosis [ 60 – 62 ].…”

Origins of Portal Hypertension in Nonalcoholic Fatty Liver Disease

“…Current strategies for the noninvasive appraisal of PHT include the use of various serum biomarkers, imaging studies, endoscopy, and liver stiffness measurements alone or in combination ( Table 1). The diagnostic performance of these methods in identifying patients with clinically significant PHT has been discussed extensively elsewhere [72][73][74][75][76]. It is important to note that these noninvasive methods have been primarily developed to predict the extent of liver fibrosis and very little is known about their ability to detect PHT that may precede cirrhosis and remains below the level of clinical significance (HVPG in the range of 5-10 mm Hg).…”

Application of the Hepatic Transit Time (HTT) in Evaluation of Portal Vein Pressure in Gastroesophageal Varices Patients

“…The reason might be that under persistent high portal vein pressure, the hepatic vessels of liver cirrhosis patients develop certain compensations, causing close connection of the hepatic artery, hepatic vein, and portal vein, and decrasing passing time of the contrast agent . On the contrary, liver tissue fibrosis, formation of regenerative nodules, and vascular obstruction can cause significant alterations in liver microcirculation, and significant elevation of local vasoconstrictors such as norepinephrine can cause hemodynamic changes in the hepatic vessels . The aforementioned aspects can cause elevations in portal vein pressure.…”