scholarly journals Brief Review of Portal Hypertension Related Complications

2021 ◽  
Author(s):  
Achyut Bikram Hamal

The pathologic increase in the pressure gradient between portal vein and inferior venacava is called portal hypertension. Increased portal blood flow and increased resistance in the portal venous system cause portal hypertension. The structural components and the functional components contribute to the resistance. Hepatic venous pressure gradient (HVPG) reflects the degree of portal pressure in liver disease. HVPG is calculated as the difference between the wedged hepatic venous pressure (WHVP) and the free hepatic venous pressure (FHVP). Clinically significant portal hypertension (CSPH) is defined as HVPG ≥10. Different values of HVPG have been defined as threshold for different consequences of portal hypertension. Variceal hemorrhage, portal hypertensive gastropathy, ascites, colopathy, biliopathy and hepatopulmonary syndrome are main complications of portal hypertension. Besides nonselective beta blockers, other drugs like statins, antioxidants, antidiabetic, anti-inflammatory and antiapoptotic drugs have also been seen to be effective in reducing portal pressure.

2020 ◽  
Vol 40 (03) ◽  
pp. 240-255 ◽  
Author(s):  
Mattias Mandorfer ◽  
Virginia Hernández-Gea ◽  
Juan Carlos García-Pagán ◽  
Thomas Reiberger

AbstractNoninvasive diagnostics for portal hypertension include imaging and functional tests, as well as blood-based biomarkers, and capture different features of the portal hypertensive syndrome. Definitive conclusions regarding their clinical utility require assessment of their diagnostic value in specific clinical settings (i.e., diagnosing a particular hemodynamic condition within a well-defined target population). Several noninvasive methods are predictive of clinically significant portal hypertension (CSPH; hepatic venous pressure gradient [HVPG] ≥ 10 mm Hg; the threshold for complications of portal hypertension); however, only a minority of them have been evaluated in compensated advanced chronic liver disease (i.e., the target population). Importantly, most methods correlate only weakly with HVPG at high values (i.e., in patients with CSPH). Nevertheless, selected methods show promise for diagnosing HVPG ≥ 16 mm Hg (the cut-off for increased risks of hepatic decompensation and mortality) and monitoring HVPG changes in response to nonselective beta-blockers or etiological treatments. Finally, we review established and potential future clinical applications of noninvasive methods.


2012 ◽  
Vol 302 (12) ◽  
pp. G1458-G1465 ◽  
Author(s):  
Eva Erice ◽  
Elba Llop ◽  
Annalisa Berzigotti ◽  
Juan G. Abraldes ◽  
Ignacio Conget ◽  
...  

Insulin resistance (IR) is involved in the pathogenesis of endothelial dysfunction and is also present in patients with cirrhosis. Intrahepatic endothelial dysfunction plays a major role, increasing hepatic vascular resistance and promoting portal hypertension (PH). In addition, β-adrenergic agonists and insulin share several intracellular signaling pathways. Thus IR may influence the response to β-blockers. This study aimed at evaluating the relationship between IR and hepatic hemodynamics in patients with cirrhosis and with the portal pressure response to acute β-blockade. Forty-nine patients with cirrhosis and PH were included. Hepatic and systemic hemodynamics were measured, and IR was estimated by using the updated homeostasis model assessment (HOMA)-2 index. Patients with HOMA-2 > 2.4 were considered IR. In patients with hepatic venous pressure gradient (HVPG) ≥ 10 mmHg) [clinically significant PH (CSPH)], hemodynamic measurements were performed again 20 min after intravenous propranolol. Mean HOMA-2 index was 3 ± 1.4. Fifty-seven percent of patients had IR. A weak correlation between HOMA-2 index and HVPG was observed. Eighty-six percent of patients had CSPH. HOMA-2 index was an independent predictor of CSPH. However, in patients with CSPH, the correlation between HOMA-2 index and HVPG was lost. HVPG, but not IR, predicted the presence of esophageal varices. Response to propranolol was not different between patients with or without IR. In nondiabetic patients with cirrhosis, HOMA-2 index is directly associated with the presence of CSPH and indirectly with varices, but does not allow either grading HVPG or predicting its response to propranolol.


Author(s):  
Fahim Ebrahimi ◽  
David Semela ◽  
Markus Heim

Abstract Background Measurement of the hepatic venous pressure gradient (HVPG) is the gold standard to evaluate the presence and severity of portal hypertension. The procedure is generally safe and well tolerated, but nevertheless, some patients demand for sedation. However, it is unknown whether propofol sedation would impair the accuracy of portal pressure measurements. Methods This is a prospective observational cohort study including cirrhotic patients with suspected portal hypertension undergoing invasive measurement of HVPG. Measurements of HVPG were performed in awake condition as well as under sedation with propofol infusion. Results In total, 37 patients were included. Mean HVPG in awake condition was 15.9 mmHg (IQR 13–19) and during sedation 14.1 mmHg (IQR 12–17). While measures of free hepatic vein pressure (FHVP) were not altered after propofol sedation (p = 0.34), wedged hepatic vein pressure values (WHVP) decreased in an average by  2.05 mmHg (95% CI − 2.46 to − 1.16; p < 0.001) which was proportional to the magnitude of HVPG. In 31 out of 37 patients (83.8%), portal hypertension with HVPG ≥ 12 mmHg was found. Under sedation with propofol, two patients (5.4%) with borderline values would have been incorrectly classified as < 12 mmHg. After adjustment for the average difference of − 10%, all patients were correctly classified. Intraclass correlation coefficient between HVPG measurement in awake condition and under propofol sedation was 0.927 (95% CI 0.594–0.975). Conclusions Propofol sedation during HVPG measurements is generally safe, however it may lead to relevant alterations of HVPG readings.


2021 ◽  
Vol 8 (3) ◽  
Author(s):  
Volkan Sarper Erikci ◽  

Normal portal pressure is between 0 and 10 mmHg and the pressure in the portal vein is slightly higher than that of the pressure in the inferior vena cava [1]. Portal Hypertension (PH) is usually defined as either a hepatice venous pressure gradient greater than 5mmHg or hepatic venous wedge pressure greater than 10mmHg [2]. It is usually encountered as a complication arising from chronic liver disease and cirrhosis. Common presentation of PH in children include catastrophic variceal hemorrhage usually from esophagus. Other common clinical features of PH include splenomegaly, hypersplenism, ascites, encephalopathy, and hepatopulmonary syndrome and portopulmonary hypertension. It has been reported that up to 15% of children with PH ultimately require shunt surgery [2]. Traditionally shunt surgery was a treatment option for children in whom control of variceal bleeding failed however; it was associated with relatively high rate of anastomotic stricture or thrombosis [1]. Nowadays it has also been reported that as the experience in vascular and transplant surgery together with microsurgical techniques have improved good success rates can be achieved even in small children [1]. In this review article, it is aimed to review the surgical treatment options in children with PH with special regard to shunt procedures under the light of relevant literature.


2021 ◽  
Vol 10 (17) ◽  
pp. 3818
Author(s):  
Alberto Zanetto ◽  
Sarah Shalaby ◽  
Paolo Feltracco ◽  
Martina Gambato ◽  
Giacomo Germani ◽  
...  

Gastrointestinal bleeding is one of the most relevant causes of death in patients with cirrhosis and clinically significant portal hypertension, with gastroesophageal varices being the most frequent source of hemorrhage. Despite survival has improved thanks to the standardization on medical treatment aiming to decrease portal hypertension and prevent infections, mortality remains significant. In this review, our goal is to discuss the most recent advances in the management of esophageal variceal hemorrhage in cirrhosis with specific attention to the treatment algorithms involving the use of indirect measurement of portal pressure (HVPG) and transjugular intrahepatic portosystemic shunt (TIPS), which aim to further reduce mortality in high-risk patients after acute variceal hemorrhage and in the setting of secondary prophylaxis.


2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Mindaugas Marozas ◽  
Romanas Zykus ◽  
Andrius Sakalauskas ◽  
Limas Kupčinskas ◽  
Arūnas Lukoševičius

Portal hypertension (PHT) is a key event in the evolution of different chronic liver diseases and leads to the morbidity and mortality of patients. The traditional reliable PHT evaluation method is a hepatic venous pressure gradient (HVPG) measurement, which is invasive and not always available or acceptable to patients. The HVPG measurement is relatively expensive and depends on the experience of the physician. There are many potential noninvasive methods to predict PHT, of which liver transient elastography is determined to be the most accurate; however, even transient elastography lacks the accuracy to be a perfect noninvasive diagnostic method of PHT. In this research, we are focusing on noninvasive PHT assessment methods that rely on selected best-supervised learning algorithms which use a wide set of noninvasively obtained data, including demographical, clinical, laboratory, instrumental, and transient elastography measurements. In order to build the best performing classification meta-algorithm, a set of 21 classification algorithms have been tested. The problem was expanded by selecting the best performing clinical attributes using algorithm-specific filtering methods that give the lowest error rate to predict clinically significant PHT. The suggested meta-algorithm objectively outperforms other methods found in literature and can be a good substitute for invasive PHT evaluation methods.


2019 ◽  
Vol 37 (6) ◽  
pp. 498-508 ◽  
Author(s):  
Carolina A. Serrano ◽  
Simon C. Ling ◽  
Sofia Verdaguer ◽  
Miguel León ◽  
Nicolás Jarufe ◽  
...  

Background/Aims: One hallmark of chronic liver disease in patients with portal hypertension is the formation of portal-systemic collaterals in which angiogenesis has a fundamental role. We studied patients with chronic liver disease undergoing liver transplantation to correlate levels of circulating angiogenic factors in portal and peripheral circulation with portal pressure and portal-systemic collaterals. Methods: Sixteen patients who underwent liver transplantation were enrolled. During transplant surgery, we determined portal venous pressure and portal-systemic collateral formation. We determined angiogenics mediator levels in systemic and portal plasma. Peripheral plasma from healthy donors was measured as controls. Results: Vascular endothelial growth factor (VEGF)-R1 and 2, Ang-1 and 2, Tie2, FGF- 1 and 2, CD163, PDGFR-β, PDGFsRα, PDGF-AB and BB, CD163, TGF-β VASH-1 levels were significantly different in the controls in comparison to cases. Significantly decreased portal venous levels of Ang-1, FGF-1, PDGF-AB/BB, and CC were observed in patients with higher portal pressure. Peripheral VEGF, Ang-1, pPDGF-AB, BB, and CC were significantly decreased in patients with more severe collateral formation. While peripheral VEGF-R1 was higher in patients with severe collateral formation. For portal circulation, VEGF, Ang-1, ­pPDGF-AB, BB, and CC were significantly decreased in patients with more severe collateral formation Conclusions: Angiogenesis factors correlated with portal pressure and collateral formation and different patterns of circulating angiogenesis mediators were found in peripheral and portal blood of patients with chronic liver disease. These results support the importance of angiogenic pathways in cirrhosis and portal hypertension and highlight areas for further study to identify clinically useful noninvasive markers of portal pressure and collateral formation.


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