MANAGEMENT OF CIRRHOTIC PATIENT (A CARDENAS AND P TANDON, SECTION EDITORS) Non-invasive Measurement of Portal Pressure Ahmed M. Elmahdy 1 & Annalisa Berzigotti 2 # Springer Science+Business Media, LLC, part of Springer Nature 2019 Abstract Purpose of Review To provide an updated overview of the existing and emerging non-invasive diagnostic methods to assess portal hypertension. Recent Findings Data on liver stiffness measurement confirmed that it is a mainstay for assessing the risk of clinically significant portal hypertension in patients with advanced chronic liver disease of any etiology. The Baveno criteria for identifying patients who can safely spare endoscopy have been validated in NASH and cholestatic liver disease. New expanded criteria and other simple non-invasive algorithms including MELD score or spleen stiffness have been proposed and can lead to a higher proportion of endoscopies without significantly increasing the risk of missing large esophageal varices. MR and CT improve the anatomical imaging of gastroesophageal varices and abdominal collaterals and dynamic imaging based on MR and able to quantify hepatic blood flow are in development. Contrast-enhanced ultrasound and methacetin breath test are emerging promising methods to estimate the HVPG non-invasively. Summary Several different non-invasive methods are now available and can be used in clinical practice to achieve a successful identification of patients with clinically significant portal hypertension in chronic liver disease. However, an exact estimation of HVPG is not available yet, and changes in portal pressure cannot yet be detected by non-invasive methods. Keywords Liver cirrhosis . Ultrasound . Elastography . Magnetic resonance . CEUS Introduction Portal hypertension (PH) is a common clinical syndrome, he- modynamically defined by an increase in the venous pressure gradient across the liver (calculated from its inflow through the portal vein versus its outflow through the hepatic veins) over 5 mmHg [1••]. Common complications of PH include the onset of gastro- esophageal varices that can increase in size and rupture leading to gastrointestinal bleeding, ascites that can further complicate with bacterial infection due to bacterial translocation from the intestine (spontaneous bacterial peritonitis) and with renal failure (hepato-renal syndrome), porto-systemic shunting leading to he- patic encephalopathy, and hypersplenism leading to thrombo- and leukocytopenia [1••]. The major cause of PH in the Western countries is advanced chronic liver disease (ACLD)/liver cirrhosis, which accounts for over 90% of cases [2]. However, other causes (schistosomiasis, extrahepatic portal vein obstruction, porto-sinusoidal disease/ idiopathic portal hypertension) are common in other geographi- cal areas of the world and should be correctly identified. Like any other vascular system, as stated by Ohm’s law, portal pressure depends upon two distinct factors: resistance to blood flow and the amount of flow (pressure = resistance × flow) [3]. The initial factor leading to the increase in portal pressure is invariably an increase in resistance to portal blood flow. This can arise at any level, i.e., at the pre-hepatic (portal vein sys- tem), intrahepatic (pre-sinusoidal, sinusoidal, or post- sinusoidal site), or post-hepatic (liver veins, inferior vena cava, right heart) level (Table 1). In cirrhosis, the increase in intrahepatic resistance occurs at a sinusoidal site, due to the structural damage through fibrogenesis, parenchymal extinction, and regeneration [2]. This article is part of the Topical Collection on Management of Cirrhotic Patient * Annalisa Berzigotti annalisa.berzigotti@insel.ch 1 Mansoura Faculty of Medicine, Mansoura, Egypt 2 Hepatology, University Clinic for Visceral Surgery and Medicine, Inselspital, University of Bern, MEM F807, Murtenstrasse 35, CH-3010 Bern, Switzerland Current Hepatology Reports https://doi.org/10.1007/s11901-019-00446-4