Portal hypertension and variceal bleeding-Unresolved issues. Summary of an American Association for the study of liver diseases and European Association for the study of the liver single-topic conference

García–Tsao, Guadalupe; Bosch, Jaime; Groszmann, Roberto J.

doi:10.1002/hep.22273

Cited by 230 publications

(170 citation statements)

References 84 publications

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“…Endoscopic therapy is an integral component of the management of acute variceal bleeding as well as prevention of recurrent bleeding [8,9]. Since it first evolved as a new therapeutic option, EBL has been regarded as a more effective modality than endoscopic injection sclerotherapy in the control of acute hemorrhage with less reported adverse events [10][11][12]. On the other hand, some studies still advocate the use of sclerotherapy as a better treatment option up to regarding it as the gold-standard treatment [13,14].…”

Section: Discussionmentioning

confidence: 99%

Management of acute esophageal variceal bleeding by endoscopic sclerotherapy in technically difficult endoscopic band ligation cases—A population based cohort study

Esmat¹,

Hamza²,

Abbas³

et al. 2013

OJGas

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Endoscopic band ligation is regarded as the main therapeutic option for acute esophageal variceal bleeding, while sclerotherapy may be used in the acute setting if ligation is technically difficult. The incidence of difficult-to-perform band ligation in acute esophageal variceal bleeding, as well as the outcome of patients subjected to injection sclerotherapy as an alternative treatment, has not been clearly investigated. Our aim is to study the outcome of patients subjected to injection sclerotherapy in the acute setting of esophageal variceal bleeding when endoscopic band ligation is technically difficult to perform. We included 151 patients with acute esophageal variceal bleeding originnating from medium or large sized varices. All patients were planned for EBL as the 1st treatment option (EBL group 61.6%), meanwhile, EIS using 5% ethanolamine oleate was reserved as the 2nd treatment option when EBL was technically difficult (EIS group 38.4%). The mean time to restore hemodynamic stability was significantly prolonged in the EIS group (11.5 ± 6.5 hrs versus 9.5 ± 5.0 hrs, p 0.05). Initial control of bleeding was significantly higher in the EBL group versus the EIS group (96.7% vs 84.5%, p 0.021). Re-bleeding was more among the EIS group (42.9% vs 24.2%, p 0.04). There were no significant differences as regarding mortality and duration of hospital stay. So, a considerable proportion of cases presenting with acute variceal bleeding will have difficulty in performing EBL. In these patients, sclerotherapy is not a waning procedure with an accepted success rate, without much additional complications and without deranging mortality.

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Section: Discussionmentioning

confidence: 99%

Management of acute esophageal variceal bleeding by endoscopic sclerotherapy in technically difficult endoscopic band ligation cases—A population based cohort study

Esmat¹,

Hamza²,

Abbas³

et al. 2013

OJGas

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“…Data on use of magnetic resonance, transient real-time elastography and ARFI appear more promising [23]. However, upper gastrointestinal tract endoscopy is still the gold standard for identifying esophageal and gastric varices, and is essential in the therapeutic management of variceal bleeding, through sclerotherapy and elastic band ligation [24].…”

Section: Varices and Bleedingmentioning

confidence: 99%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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The hyperdynamic syndrome is a late consequence of portal hypertension in cirrhosis. The principal hemodynamic manifestations of the hyperdynamic syndrome are high cardiac output, and increased heart rate and total blood volume, accompanied by reduced total systemic vascular resistance. Pathophysiology involves a complex of humoral and neural mechanisms that can determine hemodynamic changes, and lead to hyperdynamic circulation. In this review we focus our attention on the manifestations of the hyperdynamic syndrome. Some of these are well described and directly related to portal hypertension (varices, ascites, hepatic encephalopathy, and hepatorenal syndrome), while others, such as hepatopulmonary syndrome, portopulmonary hypertension, and cirrhotic cardiomyopathy, are less known as clinical manifestations related to cirrhosis and, therefore, merit further investigation.

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“…11,12 Current guidelines recommend providing prophylactic therapy to patients with varices who have any of these highrisk indicators. 13,14 In practice, this means that all patients with varices should be treated except those Child A patients with small varices without red color signs.…”

Section: The Problemmentioning

confidence: 99%

“…13,14 Metaanalysis of the many studies devoted to this issue shows that EVL is more effective in preventing bleeding, without survival benefit. 1,15,16 However, a recent Cochrane review 15 questioned this conclusion on the basis that restricting the analysis to studies with good quality standards shows no difference in bleeding rates, on the fact that these studies have a short follow-up, and on its uncertain effects in patients with relatively small varices.…”

Section: The Problemmentioning

confidence: 99%

Carvedilol for portal hypertension in patients with cirrhosis

Bosch

2010

Hepatology

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A 48-year-old male with hepatitis C-related cirrhosis is found on endoscopy to have large esophageal varices with red signs. He has never previously had variceal bleeding, and there is no evidence of hepatic encephalopathy. He does have mild ascites. Comorbidity includes diabetes which has been present for many years and is well-controlled on a stable dose of insulin. He has no cardiopulmonary disease. The hemoglobin is 12.4 g/dL, white blood cell count is 6800/mm 3 , and platelets are 112 Â 10 9 /L. Serum bilirubin is 1.8 mg/ dL, creatinine is 1.2 mg/dL, international normalized ratio is 1.3, and the serum albumin is 3.5 g/dL. The electrocardiogram and chest x-ray are normal. The ultrasound examination does not show portal vein thrombosis or hepatocellular carcinoma.What is the role of carvedilol in the prevention of variceal bleeding in this patient? How will the dose of carvedilol be adjusted and how is the patient to be monitored for adverse drug events? When would carvedilol be preferred over nadolol or propranolol? Would the approach be different if the patient was of Child-Pugh class C cirrhosis? The ProblemPortal hypertension is an almost unavoidable complication of cirrhosis, and provides the driving force for most of its complications, such as esophageal and gastric varices, variceal bleeding, portal hypertensive gastropathy, ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, thrombopenia, leukopenia and anemia, and portal-systemic encephalopathy.1 Recent studies have shown that for these complications to develop, the portacaval pressure gradient-evaluated clinically by the hepatic venous pressure gradient (HVPG)-should increase above 10 mm Hg and should be above 12 mm Hg for variceal bleeding. 2,3The prevalence of varices is about 40% in asymptomatic compensated patients.2 Development of varices follows an incidence of approximately 6% per year. The incidence is nearly double in patients with a baseline HVPG >10 mm Hg, who therefore represent a high-risk group.2 These patients are also at higher risk of developing decompensation (ascites, bleeding, jaundice, encephalopathy) and hepatocellular carcinoma. 4,5 Because of this, there is a great interest in strategies to revert portal hypertension, since these would prevent portal hypertension-related complications, clinical decompensation, and death. The benefit of reduction of HVPG has actually been proven for patients exhibiting a ''good hemodynamic response'' to nonselective beta-adrenergic blockers; i.e., those who exhibit a decrease in HVPG > 20% of baseline or to values below 12 mm Hg during continued therapy, 6,7 or who show a decrease in HVPG >10% of baseline 20 minutes after an intravenous infusion of propranolol. 8,9 Besides the increased intravascular pressure, the risk of bleeding from varices is further influenced by other factors, such as the diameter of the varices and the thickness of the variceal wall.10 These factors are interrelated by Laplace's law in the concept of wall tension (t), according to which: t ¼ variceal tran...

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Portal hypertension and variceal bleeding-Unresolved issues. Summary of an American Association for the study of liver diseases and European Association for the study of the liver single-topic conference

Cited by 230 publications

References 84 publications

Management of acute esophageal variceal bleeding by endoscopic sclerotherapy in technically difficult endoscopic band ligation cases—A population based cohort study

Management of acute esophageal variceal bleeding by endoscopic sclerotherapy in technically difficult endoscopic band ligation cases—A population based cohort study

Clinical implications of the hyperdynamic syndrome in cirrhosis

Carvedilol for portal hypertension in patients with cirrhosis

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