Variceal pressure is a factor predicting the risk of a first variceal bleeding: A prospective cohort study in cirrhotic patients

Nevens, Frederik; Bustami, Rami; Scheys, Ilse; Lesaffre, Emmanuel; Fevery, Johan

doi:10.1002/hep.510270104

Cited by 114 publications

(70 citation statements)

References 26 publications

(38 reference statements)

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“…31 In this study, variceal pressure was measured using a noninvasive technique developed in our laboratory that has been validated in other centers also. [15][16][17]32 This technique, however, has some limitations. The first and more important is that it is not feasible in every patient.…”

Section: Discussionmentioning

confidence: 99%

“…7,9 The transmural pressure at the varices can be assessed noninvasively at endoscopy using a pressure-sensitive endoscopic gauge developed in our laboratory that has been shown to allow accurate, reproducible measurements of variceal pressure. [9][10][11][12][13][14][15][16][17] Previous studies indicated that the technique allows assessment of the acute and chronic effects of drug therapy on portal hypertension. 11-15 Moreover, there is evidence suggesting that measurements of variceal pressure may have prognostic value in Abbreviations: TIPS, transjugular intrahepatic portosystemic shunt; HVPG, hepatic venous pressure gradient; WHVP, wedged hepatic venous pressure; FHVP, free hepatic venous pressure; CI, confidence interval; ROC, receiver operating characteristic curve; NIEC, North Italian Endoscopic Club index.…”

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confidence: 99%

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Predictive value of the variceal pressure response to continued pharmacological therapy in patients with cirrhosis and portal hypertension

et al. 2000

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Noninvasive measurements of variceal pressure adequately reflect the hemodynamic effects of propranolol on portal hypertension. However, the prognostic value of variceal pressure responses during continued propranolol therapy has not been evaluated, and it is unclear whether this may substitute invasive measurements of portal pressure response. Fifty-five portal hypertensive patients with cirrhosis were studied before and at 4 months of continued propranolol therapy. Variceal pressure was measured using an endoscopic pressure gauge. Portal pressure was evaluated as the hepatic venous pressure gradient (HVPG). Over a 28 ؎ 11 month follow-up, 16 patients experienced variceal bleeding. Baseline characteristics were similar in bleeders and nonbleeders. At 4 months, reduction in variceal pressure was less marked in bleeders than in nonbleeders (5% ؎ 20% vs. ؊15% ؎ 24%; P ‫؍‬ .03). A fall in variceal pressure 20% or greater of baseline was an independent predictor of absence of variceal bleeding; which occurred in 5% of patients with a 20% or greater fall in variceal pressure versus 42% of patients with less than a 20% reduction (P ‫؍‬ .004). The HVPG response had similar independent prognostic value (decrease H20%: 6% bleeding; decrease F20%: 45% bleeding; P ‫؍‬ .004) but identified different patients. Achieving a 20% decrease in either variceal pressure or HVPG was highly sensitive (85%) and specific ( Variceal bleeding is the most frequent and severe complication of portal hypertension in patients with cirrhosis. 1 Several treatment options are available to prevent recurrent variceal bleeding, including pharmacological therapy, endoscopic banding ligation, and surgical or transjugular intrahepatic portosystemic shunts (TIPS). 1,2 It has been recently shown that pharmacological treatment with propranolol offers almost optimal protection from bleeding and rebleeding when the portal venous pressure (estimated by the hepatic venous pressure gradient [HVPG]), achieves a target reduction. 3,4 The risk of bleeding or rebleeding is virtually abolished when the HVPG decreases to 12 mm Hg or below, 3-5 and the actuarial risk of rebleeding at 2 years is only 9% when the HVPG is reduced by at least 20% of the baseline value. 4 This has been thereafter confirmed by other studies, 6 emphasizing the concept that pharmacological treatment represents the optimal therapy in the subgroup of patients achieving such a pronounced decrease in HVPG. [1][2][3][4] Unfortunately, there is no adequate noninvasive way of assessing the HVPG response to treatment, which calls for repeated invasive hemodynamic studies.Several endoscopic findings, such as the size of the varices and the presence of red color signs (which are thought to reflect a reduced thickness of variceal wall) show a significant correlation with the risk of bleeding. 1,7,8 These are some of the main determinants of variceal wall tension, 7 which is believed to play a key role in determining variceal rupture. 7,9 According to Laplace' s law, variceal wall tension is directly re...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Predictive value of the variceal pressure response to continued pharmacological therapy in patients with cirrhosis and portal hypertension

et al. 2000

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“…The risk of variceal bleeding is highly dependent on portal pressure. 74 It is now accepted that associated coagulopathy whether related to the underlying liver disease or anticoagulant use does not precipitate variceal bleeding, but can make the bleeding more severe. In published studies, the overall incidence of bleeding complications with anticoagulant use in cirrhotics has been reported to vary from 5% to 35%.…”

Section: Complications Of Anticoagulation and Prophylaxis Of Varicealmentioning

confidence: 99%

Portal Vein Thrombosis in Cirrhosis

Raja

Jacob

Asthana

2014

Journal of Clinical and Experimental Hepatology

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Portal vein thrombosis (PVT) is being increasingly recognized in patients with advanced cirrhosis and in those undergoing liver transplantation. Reduced flow in the portal vein is probably responsible for clotting in the spleno-porto-mesenteric venous system. There is also increasing evidence that hypercoagulability occurs in advanced liver disease and contributes to the risk of PVT. Ultrasound based studies have reported a prevalence of PVT in 10-25% of cirrhotic patients without hepatocellular carcinoma. Partial thrombosis of the portal vein is more common and may not have pathophysiological consequences. However, there is high risk of progression of partial PVT to complete PVT that may cause exacerbation of portal hypertension and progression of liver insufficiency. It is thus, essential to accurately diagnose and stage PVT in patients waiting for transplantation and consider anticoagulation therapy. Therapy with low molecular weight heparin and vitamin K antagonists has been shown to achieve complete and partial recanalization in 33-45% and 15-35% of cases respectively. There are however, no guidelines to help determine the dose and therapeutic efficacy of anticoagulation in patients with cirrhosis. Anticoagulation therapy related bleeding is the most feared complication but it appears that the risk of variceal bleeding is more likely to be dependent on portal pressure rather than solely related to coagulation status. TIPS has also been reported to restore patency of the portal vein. Patients with complete PVT currently do not form an absolute contraindication for liver transplantation. Thrombectomy or thromboendovenectomy is possible in more than 75% of patients followed by anatomical end-to-end portal anastomosis. When patency of the portal vein and/or superior mesenteric vein is not achieved, only non-anatomical techniques (reno-portal anastomosis or cavo-portal hemitransposition) can be performed. These techniques, which do not fully reverse portal hypertension, are associated with higher morbidity and mortality risks in the short term. ( J CLIN EXP HEPATOL 2013;4:320-331)

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“…Large esophageal varices (LEV) are at a greater risk, which is possibly due to a higher variceal wall tension [7] . Availability of non-invasive methods for detection of LEV may help limit the number of endoscopic procedures.…”

Section: Introductionmentioning

confidence: 99%

Portal hemodynamics as predictors of high risk esophageal varices in cirrhotic patients

Tarzamni¹,

Somi²,

Farhang³

et al. 2008

WJG

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AIM:To evaluate portal hypertension parameters in liver cirrhosis patients with and without esophageal varices (EV). METHODS:A cohort of patients with biopsy confirmed liver cirrhosis was investigated endoscopically and with color Doppler ultrasonography as a possible noninvasive predictive tool. The relationship between portal hemodynamics and the presence and size of EV was evaluated using uni-and multivariate approaches. RESULTS:Eighty five consecutive cirrhotic patients (43 men and 42 women) were enrolled. Mean age (± SD) was 47.5 (± 15.9). Portal vein diameter (13.88 ± 2.42 vs 12.00 ± 1.69, P < 0.0005) and liver vascular index (8.31 ± 2.72 vs 17.8 ± 6.28, P < 0.0005) were found to be significantly higher in patients with EV irrespective of size and in patients with large varices (14.54 ± 1.48 vs 13.24 ± 2.55, P < 0.05 and 6.45 ± 2.78 vs 10.96 ± 5.05, P < 0.0005, respectively), while portal vein flow velocity (13.25 ± 3.66 vs 20.25 ± 5.05, P < 0.0005), congestion index (CI) (0.11 ± 0.03 vs 0.06 ± 0.03, P < 0.0005), portal hypertensive index (2.62 ± 0.79 vs 1.33 ± 0.53, P < 0.0005), and hepatic (0.73 ± 0.07 vs 0.66 ± 0.07, P < 0.001) and splenic artery resistance index (RI) (0.73 ± 0.06 vs 0.62 ± 0.08, P < 0.0005) were significantly lower. A logistic regression model confirmed spleen size (P = 0.002, AUC 0.72) and portal hypertensive index (P = 0.040, AUC 0.79) as independent predictors for the occurrence of large esophageal varices (LEV). CONCLUSION:Our data suggest two independent situations for beginning endoscopic evaluation of compensated cirrhotic patients: Portal hypertensive index > 2.08 and spleen size > 15.05 cm. These factors may help identifying patients with a low probability of LEV who may not need upper gastrointestinal endoscopy.

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Variceal pressure is a factor predicting the risk of a first variceal bleeding: A prospective cohort study in cirrhotic patients

Cited by 114 publications

References 26 publications

Predictive value of the variceal pressure response to continued pharmacological therapy in patients with cirrhosis and portal hypertension

Predictive value of the variceal pressure response to continued pharmacological therapy in patients with cirrhosis and portal hypertension

Portal Vein Thrombosis in Cirrhosis

Portal hemodynamics as predictors of high risk esophageal varices in cirrhotic patients

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