Acute variceal bleeding in patients with liver cirrhosis and portal hypertension (PHT) is the most serious emergency complication among those patients and could have catastrophic ‎outcomes if not timely managed. ‎Early screening by esophago-gastro-duodenoscopy (EGD) for the presence of esophageal varices (EVs) is ‎‎currently recommended by the practice guidelines for all cirrhotic patients. Meanwhile, EGD is not readily accepted or preferred by many patients. The literature is rich in ‎studies to investigate and validate ‎ non-invasive markers of EVs prediction aiming at reducing the unneeded endoscopic procedures. Gallbladder (GB) wall thickness (GBWT) ‎measurement has been found promising in many published research ‎articles. We aim to highlight the validity of sonographic GBWT measurement in the ‎prediction of EVs based on the available evidence.‎ We searched databases including Cochrane library, PubMed, Web of Science and many others for relevant articles. GBWT is associated with the presence of EVs in cirrhotic patients with PHT of different etiologies. The cut-off of GBWT that can predict the presence of EVs varied in the literature and ranges from 3.1 mm to 4.35 mm with variable sensitivities of 46%-90.9% and lower cut-offs in viral cirrhosis compared to non-viral, however GBWT > 4 mm in many studies is associated with acceptable sensitivity up to 90%. Furthermore, a relation was also noticed with the degree of varices and portal hypertensive gastropathy. Among cirrhotics, GBWT > 3.5 mm predicts the presence of advanced (grade III-IV) EVs with a sensitivity of 45%, the sensitivity increased to 92% when a cut-off ≥ 3.95 mm was used in another cohort. Analysis of these results should carefully be revised in the context of ascites, hypoalbuminemia and other intrinsic GB diseases among cirrhotic patients. The sensitivity for prediction of EVs improved upon combining GBWT measurement with other non-invasive predictors, e.g., platelets/GBWT.

Abnormality of hepatic vein (HV) waveforms evaluated by Doppler ultrasonography has been widely studied in patients with chronic liver disease. We investigated the correlation between changes in HV waveforms and portal vein velocity (PVVel), the hepatic artery pulsatility index (HAPI), and also the extent of abnormal Doppler HV waveforms expressed as damping index (DI), severity of portal hypertension expressed as Child-Pugh scores and portal pressure (PP) measured directly from patients with portal hypertension (PHT) to evaluate the indicative value of abnormal HV waveforms and discuss the cause of abnormal HV waveform.

Sixty patients who had been diagnosed with PHT and accepted surgical therapy of portosystemic shunts were investigated. PP was measured intraoperatively. Thirty healthy volunteers with no history of chronic liver disease were enrolled as the control group. HV waveforms were categorized as triphasic, biphasic or monophasic. DI was compared as the quantitative indicator of abnormal HV waveforms. Another two Doppler parameters, PVVel and HAPI were also measured. These Doppler features were compared with PP, Child-Pugh scores and histological changes assessed by liver biopsy.

In the patient group, the Doppler flow waveforms in the middle HV were triphasic in 31.6%, biphasic in 46.7%, and monophasic in 21.6% of subjects. These figures were 86.7%, 10.0%, and 3.3%, respectively, in healthy subjects. With the flattening of HV waveforms, the HAPI increased significantly (r = 00.438, p < 0.0001), whereas PVVel decreased significantly (r = -0.44, p <0.0001). Blood flow parameters, HAPI, PVVel and HV-waveform changes showed no significant correlations with Child-Pugh scores. The latter showed a significant correlation with PP (r = 0.589, p = 0.044). Changes of HV waveform and DI significantly correlated with PP (r = 0.579, r = 0.473, p <0.0001), and significant correlation between DI and Child-Pugh scores was observed (r = 0.411, p = 0.001). PP was significantly different with respect to nodule size (p < 0.05), but HV-waveform changes were not significantly correlated with pathological changes.

In patients with PHT, a monophasic HV waveform indicates higher portal pressure. Furthermore, quantitative indicator DI can reflect both higher portal pressure and more severe liver dysfunction. Flattening of HV waveforms accompanied by an increase in the HAPI and decrease in PVVel support the hypothesis that histological changes reducing HV compliance be the cause of abnormality of Doppler HV waveforms from the hemodynamic angle.

The purpose of this study was to investigate the relationship between a series of portal hemodynamic parameters obtained with Doppler ultrasonography and portal pressure measured directly from patients with portal hypertension (PHT).

Fifty-seven patients with a clinical diagnosis of PHT who accepted surgical therapy were investigated. The portal pressure was measured directly intraoperatively. Relevant parameters were compared and measured, including the hepatic artery pulsatility index (HAPI), hepatic artery resistive index (HARI), splenic artery resistive index, splenic artery pulsatility index (SpAPI), congestion index (CI) of the portal vein, hepatic buffer index (HBI), liver vascular index (LVI), and PHT index (PHI).

Doppler parameters for the postprandial HAPI, SpAPI, CI, LVI, HBI, and PHI were statistically different in patients with PHT and healthy control subjects (P<0.05). The portal pressure was significantly correlated with the HARI (r=0.699; P<.001), HAPI (r=0.582; P<.001), LVI (r=-0.501; P=.003), HBI (r=0.441; P=.009), and Child-Pugh scores (r=0.589; P=.044).

The HAPI, LVI, and HBI are indicative indices in patients with PHT, suggesting that color Doppler ultrasonography can be used as a noninvasive evaluation method for PHT degree. The changes in the HAPI, LVI, and HBI that accompany the increase in portal pressure can reflect hepatic resistance and hepatic artery buffer capacity accurately.

In patients with cirrhosis, the hepatic venous pressure gradient (HVPG) is the reference method for the assessment of portal hypertension (PHT). Variceal pressure (VP) may be measured at endoscopy, but its relationship to the HVPG remains controversial. The aim of the study was to retrospectively compare HVPG and VP values obtained in a cohort of patients with cirrhosis and PHT.

Within 8 days (range: 6-10 days), 64 patients in a stable condition with biopsy-proven cirrhosis [alcoholic: 47; other 17; mean age: 56.5 yrs (35-70); mean Child-Pugh's score: 9.4 +/- 1.9; ascites: 37/64; previous variceal bleeding (="bleeders"): 24/64) and oesophageal varices (grade 2: 49; grade 3: 15)] underwent both measurement of the HVPG during transjugular liver biopsy and VP at endoscopy using a "home made" pressure sensitive gauge in the absence of needle puncture of the varix. Alcoholic hepatitis was present in 28 patients with alcoholic cirrhosis.

The pressure sensitive gauge was well tolerated. The mean HVPG and VP values were 18.5 +/- 3.4 mmHg and 19 +/- 3.7 mmHg, respectively. A significant difference was observed between "bleeders" (n=24) and non "bleeders" (n=40) in terms of VP values (21.4 +/- 3.3 vs 17.2 +/- 3.2 mmHg, P<0.001), but not for HVPG values (19.4 +/- 4.1 vs 17.9 +/- 2.8 mmHg, P=0.075). A positive correlation was observed between VP and HVPG values (r=0.62, P<0.0001).

In this group of patients with cirrhosis and oesophageal varices, a "home-made" pressure sensitive gauge allowed a non invasive perendoscopic measurement of VP. The positive correlation between VP and HVPG values suggests that measurement of VP may be a reliable estimate of portal pressure in these patients.