scholarly journals Surgical Shunt Procedures in Childhood Portal Hypertension: A Review Article

2021 ◽  
Vol 8 (3) ◽  
Author(s):  
Volkan Sarper Erikci ◽  
Keyword(s):  
Portal Hypertension ◽  
Anastomotic Stricture ◽  
Venous Pressure ◽  
Relevant Literature ◽  
Portal Pressure ◽  
Vena Cava ◽  
Review Article ◽  
High Rate ◽  
Variceal Hemorrhage ◽  
Shunt Surgery

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.

scholarly journals Brief Review of Portal Hypertension Related Complications

2021 ◽  
Author(s):  
Achyut Bikram Hamal
Keyword(s):  
Portal Hypertension ◽  
Pressure Gradient ◽  
Beta Blockers ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Hepatopulmonary Syndrome ◽  
Portal Blood Flow ◽  
Variceal Hemorrhage ◽  
The Difference ◽  
Clinically Significant

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.

Portal Angiogenesis in Chronic Liver Disease Patients Correlates with Portal Pressure and Collateral Formation

2019 ◽  
Vol 37 (6) ◽  
pp. 498-508 ◽  
Author(s):  
Carolina A. Serrano ◽  
Simon C. Ling ◽  
Sofia Verdaguer ◽  
Miguel León ◽  
Nicolás Jarufe ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Portal Hypertension ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Peripheral Circulation ◽  
Chronic Liver ◽  
Noninvasive Markers ◽  
Collateral Formation

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.

Hepatic venous resistance site in the dog: localization and validation of intrahepatic pressure measurements

1987 ◽  
Vol 65 (3) ◽  
pp. 352-359 ◽  
Author(s):  
Dallas J. Legare ◽  
W. Wayne Lautt
Keyword(s):  
Blood Volume ◽  
Nerve Stimulation ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Vena Cava ◽  
Pressure Rise ◽  
Vascular Occlusion ◽  
Portal Venous Pressure ◽  
Hepatic Veins ◽  
Venous Resistance

Intrahepatic pressure (9.4 ± 0.3 mmHg; 1 mmHg = 133.32 Pa), measured proximal to a hepatic venous resistance site, was insignificantly different from portal venous pressure (9.6 ± 0.4 mmHg). This lobar venous pressure is not wedged hepatic venous pressure as it is measured from side holes in a catheter with a sealed tip. Validation of the lobar venous pressure measurement was done in a variety of ways and using different sizes and configurations of catheters. The site of hepatic venous resistance in the dog is localized to a narrow sphincterlike region about 0.5 cm in length and within 1–2 cm (usually within 1 cm) of the junction of the vena cava and hepatic veins. Sinusoidal and portal venous resistance appears insignificant in the basal state and large increases in liver blood volume (histamine infusion or passive vena caval occlusion) or large decreases in liver blood volume (passive vascular occlusion) do not alter the insignificant pressure gradient between portal and lobar venous pressures. Norepinephrine infusion (1.25 μg∙kg−1∙min−1 intraportal) and hepatic sympathetic nerve stimulation (10 Hz) led to a significantly greater rise in portal venous pressure than in lobar venous pressure, indicating some presinusoidal (and (or) sinusoidal) constriction and this indicates that lobar venous pressure cannot be assumed under all conditions to accurately reflect portal pressure. However, most of the rise in portal venous pressure induced by intraportal infusion of norepinephrine or nerve stimulation and virtually all of the pressure rise induced by histamine could be attributed to the postsinusoidal resistance site. This site was highly localized since 62% of the pressure drop from the portal vein to the inferior vena cava in the basal state occurred over a 0.5-cm length. However, the anatomical position of this site was different in the dog compared with the cat.

scholarly journals Insulin resistance in patients with cirrhosis and portal hypertension

2012 ◽  
Vol 302 (12) ◽  
pp. G1458-G1465 ◽  
Author(s):  
Eva Erice ◽  
Elba Llop ◽  
Annalisa Berzigotti ◽  
Juan G. Abraldes ◽  
Ignacio Conget ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Portal Hypertension ◽  
Endothelial Dysfunction ◽  
Intracellular Signaling ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Model Assessment ◽  
Hepatic Hemodynamics ◽  
Clinically Significant ◽  
The Relationship

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.

Urotensin II modulates hepatic fibrosis and portal hemodynamic alterations in rats

2009 ◽  
Vol 297 (4) ◽  
pp. G762-G767 ◽  
Author(s):  
William Kemp ◽  
Andrew Kompa ◽  
Arintaya Phrommintikul ◽  
Chandana Herath ◽  
Jia Zhiyuan ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Growth Factor ◽  
Hepatic Fibrosis ◽  
Transforming Growth Factor ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Hepatic Tissue ◽  
High Dose ◽  
Urotensin Ii

The influence of circulating urotensin II (UII) on liver disease and portal hypertension is unknown. We aimed to evaluate whether UII executes a pathogenetic role in the development of hepatic fibrosis and portal hypertension. UII was administered by continuous infusion over 4 wk in 20 healthy rats divided into three treatment groups, controls (saline, n = 7), low dose (UII, 1 nmol·kg−1·h−1, n = 8), and high dose (UII, 3 nmol·kg−1·h−1, n = 5). Hemodynamic parameters and morphometric quantification of fibrosis were assessed, and profibrotic cytokines and fibrosis markers were assayed in hepatic tissue. UII induced a significant dose-dependent increase in portal venous pressure (5.8 ± 0.4, 6.4 ± 0.3, and 7.6 ± 0.7, respectively, P = 0.03). High-dose UII infusion was associated with an increase in hepatic transcript for transforming growth factor-β ( P < 0.05) and platelet-derived growth factor-β ( P = 0.06). Liver tissue hydroxyproline was elevated in the high-dose group ( P < 0.05). No systemic hemodynamic alterations were noted. We concluded that UII infusion elevates portal pressure and induces hepatic fibrosis in normal rats. This response may be mediated via induction of fibrogenic cytokines. These findings have pathophysiological implications in human liver disease where increased plasma UII levels have been observed.

scholarly journals Impact of propofol sedation on the diagnostic accuracy of hepatic venous pressure gradient measurements in patients with cirrhosis

2021 ◽  
Author(s):  
Fahim Ebrahimi ◽  
David Semela ◽  
Markus Heim
Keyword(s):  
Portal Hypertension ◽  
Pressure Gradient ◽  
Hepatic Vein ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Intraclass Correlation ◽  
Hepatic Venous Pressure Gradient ◽  
Propofol Sedation ◽  
Gradient Measurements ◽  
Awake Condition

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.

Liver perfusion scintigraphy prior to and after transjugular intrahepatic portosystemic shunts (TIPS) in patients with portal hypertension

2000 ◽  
Vol 39 (05) ◽  
pp. 139-141 ◽  
Author(s):  
A. Schoniburg ◽  
K. A. Brensing ◽  
K. Reichmann ◽  
M. Bangard ◽  
B. Overbeck ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Perfusion ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Interventional Treatment ◽  
Perfusion Scintigraphy ◽  
Portosystemic Shunts ◽  
Shunt Procedure ◽  
Before And After ◽  
Intrahepatic Portosystemic Shunt

Summary Purpose: This investigation was performed to compare the hemodynamic results of the transjugular intrahepatic portosystemic shunt, a new interventional treatment for portal hypertension, with those observed after the established surgical shunt interventions. Methods: We examined 22 patients with portal hypertension due to liver cirrhosis before and after elective TIPS by liver perfusion scintigraphy. The relative portal perfusion was determined before and after the shunt procedure. Additionally, we measured the portal pressure gradient (PPG: portal-central venous pressure, mmHg). Results: Prior to TIPS, the relative portal perfusion was significantly reduced to 22 ± 9.1%. After the intervention we calculated values of 23.1 ± 10,7% in the TIPS-group (p = 0.67; not significant). In spite of unchanged portal perfusion, the portal pressure was significantly (p <0.001) reduced from 25.6 ± 5.3 to 14.8 ± 4 mm Hg. Conclusion: These results suggest that the reduction of portal hypertension by TIPS is effective. The portal perfusion is maintained by TIPS suggesting that liver perfusion is preserved to a higher degree.

Portal venous pressure and portasystemic shunting in experimental portal hypertension

1989 ◽  
Vol 257 (1) ◽  
pp. G52-G57 ◽  
Author(s):  
J. G. Geraghty ◽  
W. J. Angerson ◽  
D. C. Carter
Keyword(s):  
Portal Hypertension ◽  
Portal Vein ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Rapid Change ◽  
Quadratic Function ◽  
Portal Venous Pressure ◽  
Portal Vein Ligation ◽  
Strong Positive Correlation ◽  
The Relationship

The relationship between portal venous pressure and the degree of portasystemic shunting was studied in portal vein-ligated and cirrhotic rats anesthetized with halothane. One day after partial portal vein ligation there was a strong positive correlation (r = 0.80, n = 7) between portal pressure and shunting of mesenteric venous blood as measured by injection of radioactive microspheres. The relationship subsequently underwent rapid change but stabilized by 14 days postligation, when higher levels of shunting were again associated with higher portal pressures up to a limit of approximately 70% shunting, above which pressures did not increase further. This relationship was well described by a quadratic function (r = 0.75, n = 17). In cirrhotic rats there was no relationship between portal pressure and shunting (r = -0.01, n = 10). The results suggest that in the prehepatic model there is little inherent variability in capacity to develop shunts, which open to a degree directly related to portal pressure, but that this relationship may be altered in cirrhotic portal hypertension.

scholarly journals Assessment of a biofluid mechanics-based model for calculating portal pressure in canines

2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Jia-Yun Lin ◽  
Chi-Hao Zhang ◽  
Lei Zheng ◽  
Chen-Lu Song ◽  
Wen-Sheng Deng ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Correlation Coefficient ◽  
Likelihood Ratio ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Intraclass Correlation ◽  
Positive Likelihood Ratio ◽  
Negative Likelihood Ratio ◽  
Technical Difficulty ◽  
Biofluid Mechanics

Abstract Background Portal hypertension is a severe complication caused by various chronic liver diseases. The standard methods for detecting portal hypertension (hepatic venous pressure gradient and free portal pressure) are available in only a few hospitals due to their technical difficulty and invasiveness; thus, non-invasive measuring methods are needed. This study aimed to establish and assess a novel model to calculate free portal pressure based on biofluid mechanics. Result Comparison of each dog’s virtual and actual free portal pressure showed that a biofluid mechanics-based model could accurately predict free portal pressure (mean difference: -0.220, 95% CI: − 0.738 to 0.298; upper limit of agreement: 2.24, 95% CI: 1.34 to 3.14; lower limit of agreement: -2.68, 95% CI: − 3.58 to − 1.78; intraclass correlation coefficient: 0.98, 95% CI: 0.96 to 0.99; concordance correlation coefficient: 0.97, 95% CI: 0.93 to 0.99) and had a high AUC (0.984, 95% CI: 0.834 to 1.000), sensitivity (92.3, 95% CI: 64.0 to 99.8), specificity (91.7, 95% CI: 61.5 to 99.8), positive likelihood ratio (11.1, 95% CI: 1.7 to 72.8), and low negative likelihood ratio (0.08, 95% CI: 0.01 to 0.6) for detecting portal hypertension. Conclusions Our study suggests that the biofluid mechanics-based model was able to accurately predict free portal pressure and detect portal hypertension in canines. With further research and validation, this model might be applicable for calculating human portal pressure, detecting portal hypertensive patients, and evaluating disease progression and treatment efficacy.

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