Role of Endoscopic Ultrasound to Assess and Manage Portal Hypertension

2020 ◽  
Vol 04 (02) ◽  
pp. 103-109
Author(s):  
Sidhant Singh ◽  
Saurabh Mukewar

AbstractPortal hypertension leads to the development of varices along the gastrointestinal tract. Endoscopy plays an important role in the diagnosis and management of varices. Endosonography (EUS) enables visualization and permits access to varices and veins outside the gastrointestinal tract. EUS has emerged as an important tool, with the ability to identify vascular changes, treat gastric and ectopic varices, perform portal pressure measurements, portal venography, and intrahepatic shunt placement. This review discusses the role of endoscopy and the emerging role of EUS in evaluation and management of portal hypertension.

Diagnostics ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 1007
Author(s):  
Kazunori Nagashima ◽  
Atsushi Irisawa ◽  
Keiichi Tominaga ◽  
Ken Kashima ◽  
Yasuhito Kunogi ◽  
...  

Esophageal varices are caused by the development of collateral circulation in the esophagus as a result of portal hypertension. It is important to administer appropriate preventive treatment because bleeding varices can be fatal. Esophageal varices have complex and diverse hemodynamics, and there are various variations for each case. Endoscopic ultrasound (EUS) can estimate the hemodynamics of each case. Therefore, observation by EUS in esophageal varices provides useful information, such as safe and effective treatment selection, prediction of recurrence, and appropriate follow-up after treatment. Although treatment for the esophagogastric varices can be performed without EUS imaging, understanding the local hemodynamics of the varices using EUS prior to treatment will lead to more safe and effective treatment. EUS observation is an indispensable tool for thorough variceal care.


2021 ◽  
Vol 74 (2) ◽  
pp. 321-326
Author(s):  
Adam Kern ◽  
Tomasz Arłukowicz ◽  
Krystian Bojko ◽  
Leszek Gromadziński ◽  
Jacek Bil

Many researchers and clinicians have taken the value of hepatic venous pressure gradient (HVPG) as an essential prognostic factor in subjects with chronic liver disorders. And HVPG alterations characterize a predictive value in subjects at the beginning of the disease (HVPG 6 – 10 mmHg) as well as in subjects in whom hemodynamically significant portal hypertension has developed (HVPG ≥ 10 mmHg). Our review aims to present the feasibility and applicability of HVPG in modern clinical practice in patients with liver cirrhosis, including invasive and non-invasive methods. HVPG measurement is a feasible method with a favorable safety profile. However, hemodynamically significant portal hypertension also might be determined using non-invasive options as elastography, magnetic resonance imaging, and indices derived from laboratory parameters, e.g., aspartate aminotransferase-to-platelet ratio, platelet count/spleen diameter ratio, or VITRO score. Hepatic vein catheterization with the evaluation of HVPG is the current gold standard for determining portal pressure; however, new non-invasive techniques are nowadays more frequently used.


2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Cosmas Rinaldi A. Lesmana ◽  
Maria Satya Paramitha ◽  
Rino A. Gani

Chronic liver disease (CLD) is still a major problem, where the disease progression will lead to liver cirrhosis (LC) or hepatocellular carcinoma (HCC). Portal hypertension (PH) management and loco-regional therapy for HCC have become the cornerstones in advanced liver disease management. Recently, there are studies looking at the potential role of interventional endoscopic ultrasound (EUS) in liver diseases. EUS may be useful in vascular changes of the digestive wall evaluation, performing dynamic assessment of hemodynamic changes, predicting variceal bleeding and rebleeding risk, and assessing the pharmacological effects. In PH management, EUS-guided vascular therapy—which revolves around glue injection, endovascular coil placement/embolization, and combination of both—has shown promising results. As a diagnostic modality for liver cancer, the implementation of EUS in liver diseases is currently not only limited to liver biopsy (EUS-LB) but also in shear-wave elastography (SWE) and portal pressure gradient measurement, as well as portal vein sampling. The application of EUS-guided radiofrequency ablation (EUS-RFA) and tumor injection can also overcome the limitations shown by both modalities without EUS. Nevertheless, establishing EUS as a firm diagnostic and therapeutic modality is still challenging since the performance of interventional EUS requires high expertise and adequate facilities.


2016 ◽  
Vol 150 (4) ◽  
pp. S38
Author(s):  
Allison Schulman ◽  
Marvin Ryou ◽  
Hiroyuki Aihara ◽  
Wasif M. Abidi ◽  
Austin L. Chiang ◽  
...  

2003 ◽  
Vol 284 (3) ◽  
pp. G453-G460 ◽  
Author(s):  
Yukihiro Yokoyama ◽  
Hongzhi Xu ◽  
Nicole Kresge ◽  
Steve Keller ◽  
Amir H. Sarmadi ◽  
...  

Although the mechanisms of cirrhosis-induced portal hypertension have been studied extensively, the role of thromboxane A2 (TXA2) in the development of portal hypertension has never been explicitly explored. In the present study, we sought to determine the role of TXA2 in bile duct ligation (BDL)-induced portal hypertension in Sprague-Dawley rats. After 1 wk of BDL or sham operation, the liver was isolated and perfused with Krebs-Henseleit bicarbonate buffer at a constant flow rate. After 30 min of nonrecirculating perfusion, the buffer was recirculated in a total volume of 100 ml. The perfusate was sampled for the enzyme immunoassay of thromboxane B2(TXB2), the stable metabolite of TXA2. Although recirculation of the buffer caused no significant change in sham-operated rats, it resulted in a marked increase in portal pressure in BDL rats. The increase in portal pressure was found concomitantly with a significant increase of TXB2 in the perfusate (sham vs. BDL after 30 min of recirculating perfusion: 1,420 ± 803 vs. 10,210 ± 2,950 pg/ml; P < 0.05). Perfusion with a buffer containing indomethacin or gadolinium chloride for inhibition of cyclooxygenase (COX) or Kupffer cells, respectively, substantially blocked the recirculation-induced increases in both portal pressure and TXB2 release in BDL group. Hepatic detection of COX gene expression by RT-PCR revealed that COX-2 but not COX-1 was upregulated following BDL, and this upregulation was confirmed at the protein level by Western blot analysis. In conclusion, these results clearly demonstrate that increased hepatic TXA2 release into the portal circulation contributes to the increased portal resistance in BDL-induced liver injury, suggesting a role of TXA2 in liver fibrosis-induced portal hypertension. Furthermore, the Kupffer cell is likely the source of increased TXA2, which is associated with upregulation of the COX-2 enzyme.


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