Materiały źródłowe

• #1 Esophageal Varices – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK448078/

  Esophageal varices are dilated submucosal distal esophageal veins connecting the portal and systemic circulations. They form due to portal hypertension, which commonly is a result of cirrhosis, resistance to portal blood flow, and increased portal venous blood inflow. Variceal rupture is the most common fatal complication of cirrhosis. the severity of liver disease correlates with the presence of varices and risk of bleeding. […] Esophageal varices are dilated submucosal distal esophageal veins connecting the portal and systemic circulations. This happens due to portal hypertension (most commonly a result of cirrhosis), resistance to portal blood flow, and increased portal venous blood inflow. The most common fatal complication of cirrhosis is variceal rupture; the severity of liver disease correlates with the presence of varices and risk of bleeding.

• #2 Pathophysiology of Portal Hypertension and Esophageal Varices

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3362051/

  Esophageal varices are the major complication of portal hypertension. It is detected in about 50% of cirrhosis patients, and approximately 515% of cirrhosis patients show newly formed varices or worsening of varices each year. […] Optimal management of esophageal varices requires a clear understanding of the pathophysiology and natural history. […] Portal hypertension is associated with both increased portal inflow and increased outflow resistance. […] Portal hypertension results in the development of collateral vessels, which are the route blood returning to the systemic circulation from portal system bypassing the liver. […] Varices are closely associated with the condition of HVPG higher than 12mmHg. […] Patients with an HVPG 20mmHg measured within 24 hours of variceal bleeding have been identified as being at a higher risk for early rebleeding or failure to control bleeding.

• #3 Esophageal Varices – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK448078/

  Portal hypertension causes portocaval anastomosis to develop to decompress portal circulation. Normal portal pressure is between 5-10 mmHg but in the presence of portal obstruction, the pressure may be as high as 15-20 mmHg. Since the portal venous system has no valves, resistance at any level between the splanchnic vessels and right side of the heart results in retrograde flow and elevated pressure. The collaterals slowly enlarge and connect the systemic circulation to the portal venous system. Over time, this leads to a congested submucosal venous plexus with tortuous dilated veins in the distal esophagus. Variceal rupture results in hemorrhage. […] Increased resistance to portal flow at the level of hepatic sinusoids is caused by intrahepatic vasoconstriction due to decreased nitric oxide production, and increased release of endothelin-1 (ET-1), angiotensinogen, and eicosanoids. Sinusoidal remodeling disrupting blood flow. […] Increased portal flow is caused by hyperdynamic circulation due to splanchnic arterial vasodilation through mediators such as nitric oxide, prostacyclin, and TNF.

• #4 Pathogenesis of variceal bleeding in patients with cirrhosis – UpToDate

  https://www.uptodate.com/contents/pathogenesis-of-variceal-bleeding-in-patients-with-cirrhosis

  Pathogenesis of variceal bleeding in patients with cirrhosis […] A major cause of cirrhosis-related morbidity and mortality is the development of variceal bleeding, a direct consequence of portal hypertension. […] This topic will review the pathogenesis of variceal bleeding including the formation and progression of varices. […] Portal pressure is determined by the product of portal flow volume and resistance to outflow from the portal vein. Portal hypertension (defined as hydrostatic pressure >5 mmHg) results initially from increased resistance to portal venous outflow. Obstruction may occur at a presinusoidal (eg, portal vein thrombosis, portal fibrosis, or infiltrative lesions), sinusoidal (cirrhosis), or postsinusoidal (eg, sinusoidal obstruction syndrome, Budd-Chiari syndrome) level. Cirrhosis is the most common cause of portal hypertension; in these patients, elevated portal pressure results from both increased resistance to outflow through distorted hepatic sinusoids, and enhanced portal inflow due to splanchnic arteriolar vasodilation. […] Varices develop in order to decompress the hypertensive portal venous system into the systemic circulation. They are seen when the pressure gradient between the portal and hepatic veins rises above 10 mmHg; patients with values ≥12 mmHg are at risk for variceal bleeding.

• #5 Management of gastroesophageal varices in cirrhotic patients: current status and future directions | Annals of Hepatology

  https://www.elsevier.es/en-revista-annals-hepatology-16-articulo-management-gastroesophageal-varices-in-cirrhotic-S1665268119306507

  Portal hypertension plays a key role in the development of cirrhosis-associated complications, such as ascites, hepatic encephalopathy, and gastroesophageal varices (GEV). […] Measurement of the hepatic venous pressure gradient (HVPG) is standard for estimating portal pressure. Portal hypertension is defined as HVPG 5 mmHg. HVPG 10 mmHg is considered clinically significant portal hypertension (CSPH) and can result in the formation of GEV. […] Studies have reported that GEV develops in approximately 50% of cirrhotic patients and that bleeding from esophageal varices (EV) and gastric varices (GV) occurs in approximately 25% of patients at 2 years and 10 to 16% at 1 year. […] A study of hepatitis C virus (HCV)-related compensated cirrhosis found that the presence of EV is a predictor of hepatic decompensation and mortality.

• #6 Diagnosis and Management of Esophagogastric Varices

  https://www.mdpi.com/2075-4418/13/6/1031

  Portal hypertension (PH) develops as a consequence of increased resistance to portal flow and is enhanced by the presence of increased portal collateral blood flow. […] The increased resistance is mainly due to a combination of structural changes (distortion of the liver microcirculation by fibrosis, nodules, angiogenesis, and vascular occlusion) and dynamic changes (increased release of vasoconstrictors as angiotensin-II, norepinephrine, thromboxane A2 and endothelins, and the reduced production of vasodilators as nitric oxide). […] Esophageal varices develop as a result of PH, which is traditionally assessed indirectly by determining the hepatic venous pressure gradient (HVPG): PH is defined as an HVPG > 5 mmHg, while CSPH is defined in presence of a gradient > 10 mmHg.

• #7 Beta blockers in portal hypertension. Are they really a good option? | Annals of Hepatology

  https://www.elsevier.es/en-revista-annals-hepatology-16-articulo-beta-blockers-in-portal-hypertension–S166526811932023X

  Non-selective beta blockers are very useful drugs in preventing first variceal bleeding and re-bleeding in patients with cirrhosis. These drugs work in two ways: 1) by blocking 1 receptors and reducing cardiac output, and 2) by blocking 2 receptors, producing splanchnic vasoconstriction and reducing portal flow. Consequently, they reduce portal pressure. […] In the physiopathology of portal hypertension, there is an increase in portal blood flow due to splanchnic vasodilatation. Moreover, there is intrahepatic resistance to this blood flow, the first known mechanism of portal hypertension. This is due not only to an alteration in hepatic architecture, but also to a dynamic situation originating in the contraction of perivascular smooth muscle cells, myofibroblasts, and hepatic stellate cells, which represent approximately 30% of global intrahepatic resistance, this concept first described by Bathal and Groszmann.

• #8 Clinical and Molecular Hepatology

  https://www.e-cmh.org/m/journal/view.php?number=1394

  Gastroesophageal varices (GEVs) are frequent complication of liver cirrhosis and a leading cause of mortality in patients with liver cirrhosis. […] Portal hypertension, which is the most common complication of liver cirrhosis, is the main determinant for development of GEVs. Increased intrahepatic vascular resistance to portal flow leads to the development of portal hypertension, which is aggravated by splanchnic vasodilatation and increase in portal blood flow by hyperdynamic circulation. […] When the portal pressure increases above a threshold, collaterals develop at the site of communication between the portal and systemic circulation. […] In this condition, GEVs are the most important collaterals, and with the aggravation of portal hypertension, they grow and eventually rupture. […] Bleeding from GEVs is a major complication of portal hypertension and a leading cause of mortality in patients with liver cirrhosis.

• #9 Esophageal varix | Radiology Reference Article | Radiopaedia.org

  https://radiopaedia.org/articles/oesophageal-varix?lang=us

  Esophageal varices describe dilated submucosal veins of the esophagus, and are an important portosystemic collateral pathway. They are typically caused by portal hypertension, as a collateral pathway between the portal vein and the superior vena cava (via the azygos vein). The most common cause of this phenomenon is cirrhosis secondary to alcohol excess, however less common etiologies include primary biliary cholangitis, primary sclerosing cholangitis, portal vein thrombosis, Budd-Chiari syndrome, and schistosomiasis. Additionally, patients will often have stigmata of portal hypertension and cirrhosis the most common etiological basis for esophageal varices. […] Downhill esophageal varices are typically caused by superior vena cava obstruction, as part of superior vena cava syndrome, as a collateral pathway between the superior vena cava into the portal circulation and/or the inferior vena cava.

• #10 Pathophysiology of Portal Hypertension and Esophageal Varices

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3362051/

  The development of portal-collateral circulation is one of the hemodynamic features of portal hypertension. Formation of collaterals is a complex process involving the opening, dilatation, and hypertrophy of preexisting vascular channels. […] The vascular resistance of collateral vessels may be a major component of the overall resistance to portal blood flow and, therefore, may be important in determining portal pressure. […] The endothelium under normal condition has a function to produce vasodilators in response to increases in blood volume and blood pressure or to produce vasoconstrictors to prevent or attenuate the concomitant increase in pressure. However, abnormality in the endothelium-related vascular reaction occurs in several pathologic conditions, that is, endothelial dysfunction. […] The pathophysiology in portal hypertension is likely to be multifactorial in origin; various interactive regulations may be present to compensate for the effect of vasoactive mediators.

• #11 Portal Hypertension: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/182098-overview

  The portal vein carries approximately 1500 mL/min of blood from the small and large bowel, the spleen, and the stomach to the liver. […] Obstruction of portal venous flow, whatever the etiology, results in a rise in portal venous pressure. […] The response to increased venous pressure is the development of collateral circulation that diverts the obstructed blood flow to the systemic veins. These portosystemic collaterals form by the opening and dilatation of preexisting vascular channels connecting the portal venous system and the superior and inferior vena cava. […] Although high portal pressure is the main cause of the development of portosystemic collaterals, other factors, such as active angiogenesis, may also be involved. The most important portosystemic anastomoses are the gastroesophageal collaterals, which include esophageal varices. The gastroesophageal collaterals drain into the azygos vein.

• #12 Management of gastroesophageal varices in cirrhotic patients: current status and future directions | Annals of Hepatology

  https://www.elsevier.es/en-revista-annals-hepatology-16-articulo-management-gastroesophageal-varices-in-cirrhotic-S1665268119306507

  Bleeding from gastroesophageal varices (GEV) is a serious event in cirrhotic patients and can cause death. According to the explosion theory, progressive portal hypertension is the primary mechanism underlying variceal bleeding. […] Increased portal inflow is induced by mesenteric arterial vasodilatation, and its underlying mechanism involves the enhanced expression of vasodilators, including nitric oxide (NO) and glucagon. Increased resistance to portal outflow is caused by mechanical obstruction of flow by intrahepatic fibrous tissue and intrahepatic vasoconstriction; the mechanism for the latter involves the synergistic effect of the increased expression of vasoconstrictors, such as endothelin, angiotensinogen and eicosanoids, and the decreased expression of vasodilators, including NO and carbon monoxide.

• #13 Gastrointestinal varices pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Gastrointestinal_varices_pathophysiology

  Varices arise from hemodynamic disturbance between the systemic and portal venous system. The majority of venous drainage of the gastrointestinal system occurs via the portal venous system. Whenever there is an interruption of drainage through the portal system (for example due to cirrhosis), the vessels contributing to the porto-caval shunts become more prominent due to increased pressure gradient. The interruption in blood flow leads to the creation collateral vessels that involve veins of the esophagus, stomach, pelvis (hemorrhoids), retroperitoneum, liver, abdominal wall, and other areas. […] Esophageal varices are a major complication of portal hypertension (increased blood pressure in the portal venous system). In order to understand the mechanism leading to the development of esophageal varices, it is important to understand the normal vascular architecture and venous drainage of the esophagus.

• #14 Beta blockers in portal hypertension. Are they really a good option? | Annals of Hepatology

  https://www.elsevier.es/en-revista-annals-hepatology-16-articulo-beta-blockers-in-portal-hypertension–S166526811932023X

  By employing hepatic vein pressure gradient (HVPG = wedged hepatic pressure-free hepatic pressure) as a portal pressure reflex, it is known that an HVPG of 10 mmHg is required for esophageal varices to appear, and an HVPG of over 12 mmHg is a requirement for these varices to bleed. […] More than 40% of patients with cirrhosis have esophageal varices at the moment of diagnosis. Approximately 30% of these patients with large varices will experience a bleeding episode in the subsequent 2 years, with a 1-year re-bleeding possibility of approximately 60% and mortality of 20% in each episode. […] Propranolol and nadolol, which are non-selective beta blockers, reduce portal pressure via two mechanisms: 1) Cardiac output is reduced by blocking 1 adrenergic receptors, 2) Splachnic vasoconstriction by blocking 2 receptors (vasodilators).

• #15 Esophageal varices – Wikipedia

  https://en.wikipedia.org/wiki/Esophageal_varices

  Esophageal varices are extremely dilated sub-mucosal veins in the lower third of the esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis. People with esophageal varices have a strong tendency to develop severe bleeding which left untreated can be fatal. […] The lower one third of the esophagus is drained into the superficial veins lining the esophageal mucosa, which drain into the left gastric vein, which in turn drains directly into the portal vein. These superficial veins (normally only approximately 1 mm in diameter) become distended up to 12 cm in diameter in association with portal hypertension. […] If the portal pressure rises above 12 mmHg, this gradient rises to 710 mmHg. A gradient greater than 5 mmHg is considered portal hypertension. At gradients greater than 10 mmHg, blood flowing through the hepatic portal system is redirected from the liver into areas with lower venous pressures. This means that collateral circulation develops in the lower esophagus, abdominal wall, stomach, and rectum. The small blood vessels in these areas become distended, becoming more thin-walled, and appear as varicosities. […] In situations where portal pressures increase, such as with cirrhosis, there is dilation of veins in the anastomosis, leading to esophageal varices.

• #16 Esophageal varices – wikidoc

  https://www.wikidoc.org/index.php/Esophageal_varices

  In medicine (gastroenterology), esophageal varices are extremely dilated sub-mucosal veins in the esophagus. They are most often a consequence of portal hypertension, such as may be seen with cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding. […] The majority of blood from the esophagus is drained away via the esophageal veins, which drain deoxygenated blood from the esophagus to the azygos vein which in turn, directly drains into the superior vena cava. These veins have no part in the development of esophageal varices. The remaining blood from the esophagus is drained away via the superficial veins lining the esophagus interior, which drain into the coronary vein (left gastric vein) which in turn, drains directly into the portal vein. These superficial veins lining the esophagus interior (normally only approximately 1mm in diameter) become distended up to 1-2 cm in diameter in association with portal hypertension.

• #17 Esophageal varices – wikidoc

  https://www.wikidoc.org/index.php/Esophageal_varices

  Normal portal pressure is approximately 9 mmHg compared to an inferior vena cava pressure of 2-6 mmHg. This creates a normal pressure gradient of 3-7 mmHg. If the portal pressure rises above 12mmHg, this gradient rises to 7-10 mmHg. A gradient greater than 10 mmHg is considered portal hypertension. At gradients greater than 10 mmHg, blood flow though the hepatic portal system is redirected from the liver into areas with lower venous pressures. This means that collateral circulation develops in the lower esophagus, abdominal wall, stomach and rectum. The small blood vessels in these areas become distended, becoming more thin-walled, and appear as varicosities. In addition, these vessels are poorly supported by other structures, as they are not designed for high pressures. […] In situations where portal pressures increase, such as with cirrhosis, there is dilation of veins in the anastomosis, leading to esophageal varices.

• #18 Esophageal Varices: Symptoms, Causes & Treatment

  https://my.clevelandclinic.org/health/diseases/15429-esophageal-varices

  Cirrhosis of the liver is the usual cause of portal vein hypertension, which makes esophageal varices swell. […] Esophageal varices are a direct consequence of portal hypertension, which is high blood pressure in your portal venous system. This includes the portal vein that runs through your liver and the smaller veins that branch off from it, sending blood back to your heart and into general circulation in your body. […] Your body compensates for portal hypertension by redirecting blood flow into smaller veins that arent designed to handle the greater volume. The smallest of these, with the thinnest walls, become enlarged. These veins are in the mucous lining of your gastrointestinal tract: your esophagus, stomach and anus. […] Pressure gradually increases until a rupture occurs. There doesnt seem to be any precipitating event, but rupture usually occurs when blood pressure in the vein has risen by 50% to 100%. Varices that bleed are usually larger than 5 millimeters. Smaller varices reach this size at an average rate of 8% each year.

• #19 Gastrointestinal varices pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Gastrointestinal_varices_pathophysiology

  Portal hypertension develops due to the formation of porto-collateral circulation. […] Dilatation and hypertrophy of preexisting vascular channels lead to the formation of these collateral channels. […] Collaterals develop according to the increased portal pressure, and minimum threshold level of hepatic-venous portal gradient may be 10mmHg for the development of porto-systemic collaterals and esophageal varices. […] The wall tension of the vessel determines if there will be rupture of the varices. The wall tension depends upon the variceal pressure, luminal pressure and radius of the vessel. […] When the wall tension overcomes the elastic limit of the varices, rupture occurs.

• #20 esophageal-gastric-varices | Calgary Guide

  https://calgaryguide.ucalgary.ca/esophageal-gastric-varices/esophageal-gastric-varices-final/

  Pre Hepatic Portal Hypertension Hypertension *Hypercoagulable states such as thrombophilia, malignancy, or connective tissue disease Portal esophageal/gastric Esophageal/Gastric blood flow backed anastomoses up into Varices As variceal pressure 1` vessels swell 4 Blood loss from circulation 1 vessel J, wall thickness 1 vessel size tension Dilation of veins in submucosa.

• #20 esophageal-gastric-varices | Calgary Guide

  https://calgaryguide.ucalgary.ca/esophageal-gastric-varices/esophageal-gastric-varices-final/

  Esophageal/Gastric Varices: Pathogenesis and clinical findings Schistosomiasis Schistosoma species enter the body through the skin and circulate to liver Eggs lodge in terminal portal venules causing inflammation and fibrosis 1` resistance through fibrosed and inflamed sinusoids Cirrhosis Liver disease activates hepatic stellate cells causing hepatic fibrosis I` resistance through fibrosed and distorted sinusoids 1` portal inflow due to splanchnic vasodilation Veno-Occlusive Disease Budd-Chiari Syndrome Endothelial damage Hypercoagulable in the sinusoids leads to clotting states* cause factor deposition in thrombosis of hepatic sinusoids hepatic veins 1` resistance t resistance through through hepatic occluded distal veins occluded sinusoids by thrombus […] Intra Hepatic Portal Hypertension Post Hepatic Portal Portal Vein Thrombosis Hypercoagulable states* cause thrombosis of portal vein Infiltrative Lesion Primary or secondary malignancy localized to the portal vein Splenic Vein Thrombosis Pancreatitis leads to inflammation and thrombosis of the splenic vein 1 resistance through 1 resistance through 1` resistance through portal vein occluded portal vein occluded by splenic vein occluded by thrombus malignancy by thrombus

• #21 Clinical and Molecular Hepatology

  https://www.e-cmh.org/m/journal/view.php?number=1547

  Increase in portal pressure stimulates the release of angiogenic factors such as vascular endothelial growth factor and placental growth factor from the vascular beds of the splanchnic circulation, which promotes angiogenesis leading to formation of portosystemic collaterals. […] Portosystemic collaterals also formed by the opening, dilatation, and hypertrophy of existing blood vessels in the setting of increased portal pressure. […] LC patients also have a hyperdynamic circulation defined as high blood volume/high cardiac output but low effective blood volume due to low systemic vascular resistance caused by systemic vasodilatation. This hyperdynamic circulation further aggravates PH and variceal development. […] Risk factors for EV bleeding include varices located in critical area (EV bleeding commonly occurs at 3 cm proximal to the gastroesophageal junction), high portal pressure (decreasing HVPG to 12 mmHg or less lowers the risk of variceal bleeding), large size varices, blue coloration, and the presence of red-color signs. […] GV, on the other hand, can be present in the setting of lower portal pressure compared to EV. Large size varices (more than 5 mm in diameter), red-color signs, and advanced stage of liver disease (CP class B or C) are considered as the most important risk factors for GV bleeding.

• #22 Portal Hypertension: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/182098-overview

  An elevated pressure difference between systemic and portal circulation (ie, HVPG) directly contributes to the development of varices. […] The hypertensive portal vein is decompressed by diverting up to 90% of the portal flow through portosystemic collaterals back to the heart, resulting in enlargement of these vessels. These vessels are commonly located at the gastroesophageal junction, where they lie subjacent to the mucosa and present as gastric and esophageal varices. Varices form when the HVPG exceeds 10 mm Hg; they usually do not bleed unless the HVPG exceeds 12 mm Hg (normal HVPG: 1-5 mm Hg). […] Increased portal pressure contributes to increased varix size and decreased varix wall thickness, thus leading to increased variceal wall tension. Rupture occurs when the wall tension exceeds the elastic limits of the variceal wall. Varices are most superficial at the gastroesophageal junction and have the thinnest wall in that region; thus, variceal hemorrhage invariably occurs in that area.

• #23 English | World Gastroenterology Organisation

  https://www.worldgastroenterology.org/guidelines/esophageal-varices/esophageal-varices-english

  Esophageal varices are Porto-systemic collaterals i.e., vascular channels that link the portal venous and the systemic venous circulation. They form as a consequence of portal hypertension (a progressive complication of cirrhosis), preferentially in the sub mucosa of the lower esophagus. […] Rupture and bleeding from esophageal varices are major complications of portal hypertension and are associated with a high mortality rate. Variceal bleeding accounts for 1030% of all cases of upper gastrointestinal bleeding. […] The presence of gastroesophageal varices correlates with the severity of liver disease. […] As portal pressure increases, the patient may progress to having small varices. With time, and as the hyperdynamic circulation increases, blood flow through the varices will increase, thus raising the tension in the wall. Variceal hemorrhage resulting from rupture occurs when the expanding force exceeds the maximal wall tension. If there is no modification in the tension of the wall, there will be a high risk of recurrence.

• #24 Pathogenesis of Portal Hypertension and Esophageal Varices

  https://smj.journals.ekb.eg/article_39061.html

  Esophageal varices are the major complication of portal hypertension. It is detected in about 50% of cirrhosis patients. Portal hypertension is associated with both increased portal inflow and increased intrahepatic vascular resistance. Intrahepatic vascular resistance is caused by the architectural distortion of the liver resulting from fibrosis and by increased sinusoidal tone. Portal venous inflow results from a combination of a hyperdynamic circulatory state and increased plasma volume. In response to the increased portal pressure, collateral circulation develops by the opening of preexisting vascular channels. Esophagogastric varices are the most important collateral vessels: they tend to increase in size with the increase of portal pressure and rupture when wall tension exceeds a critical value.

• #25 Esophageal Varices: Symptoms, Causes & Treatment

  https://my.clevelandclinic.org/health/diseases/15429-esophageal-varices

  The most common cause is cirrhosis of the liver. Cirrhosis means scarring. This is the result of long-term, chronic liver damage. Constant inflammation (hepatitis) in your liver tissues eventually turns them into scar tissue, which blocks the flow of blood through the portal vein. This is a gradual process that usually takes decades.

• #26 Esophageal varices – Wikiwand

  https://www.wikiwand.com/en/articles/esophageal_varices

  In situations where portal pressures increase, such as with cirrhosis, there is dilation of veins in the anastomosis, leading to esophageal varices. Splenic vein thrombosis is a rare condition that causes esophageal varices without a raised portal pressure. […] Varices can also form in other areas of the body, including the stomach (gastric varices), duodenum (duodenal varices), and rectum (rectal varices).

• #27 Clinical and Molecular Hepatology

  https://www.e-cmh.org/m/journal/view.php?number=1394

  Therefore, prevention of variceal development and progression, prevention of bleeding from GEV, appropriate management for acute bleeding from GEV, and prevention of variceal rebleeding are critical in patients with liver cirrhosis. […] The main risk factor of variceal development in these patients is a hepatic venous pressure gradient (HVPG) 10 mmHg. […] The independent risk factors of progression of EVs are alcoholic cirrhosis, decompensated disease (Child-Pugh class B/C), the presence of red color sign at first endoscopy, and splenomegaly. […] A previous study suggested that HVPG is significantly associated with the risk of rebleeding and patients with HVPG 20 mmHg within 24 hours of variceal bleeding have higher risk of recurrent bleeding within 1 week and higher risk of failure in bleeding control.

• #28 English | World Gastroenterology Organisation

  https://www.worldgastroenterology.org/guidelines/esophageal-varices/esophageal-varices-english

  An international normalized ratio (INR) score 1.5, a portal vein diameter of 13 mm, and thrombocytopenia have been found to be predictive of the likelihood of varices being present in cirrhotics. […] The use of vasoactive drugs may be safe and effective whenever endoscopic therapy is not promptly available and is associated with less adverse events than emergency sclerotherapy. […] Endoscopic sclerotherapy and variceal band ligation are effective in stopping bleeding in up to 90% of patients. […] A transjugular intrahepatic portosystemic shunt (TIPS) is a good alternative when endoscopic treatment and pharmacotherapy fail. […] Terlipressin reduces failure to control bleeding and mortality, and should be the first choice for pharmacological therapy when available.

• #29 Prediction of esophageal varices in patients with HCV-related cirrhosis using albumin-bilirubin, platelets-albumin-bilirubin score, albumin-bilirubin-platelets grade, and GAR | Egyptian Liver Journal | Full Text

  https://eglj.springeropen.com/articles/10.1186/s43066-020-00027-x

  Development of esophageal varices (EVs) is the main complication of portal hypertension. […] Esophageal varices (EVs), a major complication of portal hypertension, may rupture and bleed with increased mortality rate. EVs are dilated tortuous submucosal veins usually in the distal esophagus. They develop when HVPG 10 mmHg but bleed when HVPG 12 mmHg. […] Liver cirrhosis is the most important cause of portal hypertension. There are several factors associated with pathogenesis of portal hypertension. There is increased intrahepatic vascular resistance to the portal flow due to sinusoidal capillarization as well as fibrosis-induced distortion of the vasculature. Dynamically, there is contraction of the smooth muscles of the blood vessels, hepatic stellate cells around the sinusoids, and the myofibroblasts in the fibrous septae, in response to increased vasoconstrictors, e.g., endothelins, norepinephrine, angiotensin II, cysteinyl leukotrienes and decreased intrahepatic vasodilators as nitrous oxide. Splanchnic vasodilation in response to glucagon, nitrous oxide, prostacyclin, bacterial translocation, and carbon monoxide is a major cause of increased portal venous flow.

• #30

  https://xiahepublishing.com/2310-8819/JCTH-2023-00061

  Portal hypertension refers to a group of clinical syndromes caused by elevated pressure in the portal venous system due to different causes, the most common of which is liver cirrhosis. […] The basic pathophysiological features of portal hypertension include obstruction of blood flow and/or increased blood flow in the portal venous system, increased static pressure in the portal vein and its tributaries, and the formation of collateral circulation. […] Liver cirrhosis of any etiology can induce portal hypertension; portal pressure is the product of intrahepatic vascular resistance along with portal blood flow. […] In liver cirrhosis, there is a large amount of neovascularization and sinusoidal hepatic capillarization in the area of hepatic fibrosis, resulting in increased intrahepatic blood flow and resistance.

• #31 Carvedilol delays the progression of small oesophageal varices in patients with cirrhosis: an unmet need finally met? – Gohar – AME Medical Journal

  https://amj.amegroups.org/article/view/3765/html

  Non-selective beta blocker (NSBB) therapy remains the front runner in the treatment of portal hypertension. […] NSBBs used in clinical practice are propranolol, nadolol and carvedilol. They act to reduce portal hypertension through 1 blockade and lowering cardiac output and 2 blockade leading to splanchnic vasoconstriction through unopposed 1 action. This results in reduced splanchnic inflow and portal pressure. Carvedilol additionally acts as a vasodilator due to its 1 receptor blockade effect which reduces porto-collateral resistance. Its actions on hepatic stellate cells lead to a reduction in intrahepatic resistance. […] There is emerging data showing that prior to the development of clinically significant portal hypertension (CSPH) defined as hepatic venous pressure gradient (HVPG) 10 mmHg, the effect of NSBBs on reduction of portal pressure is negligible. The hypothesis is that at lower portal pressures, increased intrahepatic resistance rather than splanchnic vasodilatation accounts for portal hypertension. Intrahepatic resistance is not amenable to most NSBBs apart from carvedilol.

• #32 Beta blockers in portal hypertension. Are they really a good option? | Annals of Hepatology

  https://www.elsevier.es/en-revista-annals-hepatology-16-articulo-beta-blockers-in-portal-hypertension–S166526811932023X

  Previous reports demonstrated that reducing HVPG to less than 12 mmHg nearly totally lowers risk of bleeding. […] Other studies have shown that even without reaching these values, reducing HVPG by at least 20% of the basal value is related with lower bleeding risk, estimated at between 4 and 9% in 1 and 2 years, respectively. […] Once the hemodynamic goal is reached, it is sustained in the majority of patients. […] Hemodynamic response is achieved independently from lowering heart rate to fewer than 55 beats per minute. […] The best treatment option for patients in whom combination therapy is not effective remains unknown to date. […] Endoscopic banding is effective, but for a short time only because portal pressure and flow are not modified and there is a recurrence of varices up to 50% in 2 years.

• #33 Pathophysiology and management of esophageal varices in current p | 62391

  https://www.primescholars.com/proceedings/pathophysiology-and-management-of-esophageal-varices-in-current-practice-62391.html

  Esophageal varices are dilated submucosal distal esophageal veins connecting the portal and systemic circulations. This happens due to portal hypertension (most commonly a result of cirrhosis), resistance to portal blood flow, and increased portal venous blood inflow. […] Esophageal varices are one of the most common and severe complications of chronic liver disease. New aspects in epidemiology, pathogenesis, and treatment of varices are reviewed. […] Prophylactic ligation should be considered for patients with large esophageal varices who cannot tolerate β blockers. Subsequent research should further compare ligation and β blockers to determine the effect on mortality, and measure ligations cost-effectiveness.

• #34

  https://journals.lww.com/co-gastroenterology/abstract/1992/08000/pathophysiology_and_management_of_esophageal.6.aspx

  Esophageal varices are one of the most common and severe complications of chronic liver disease. […] New aspects in epidemiology, pathogenesis, and treatment of varices are reviewed. […] However, prophylactic treatment regimens do not have a major impact on survival.

• #35 Bleeding esophageal varices: Who should receive a shunt? | Cleveland Clinic Journal of Medicine

  https://www.ccjm.org/content/84/3/199

  Cirrhosis of the liver alters the hepatic architecture. Development of regenerating nodules and deposition of connective tissue between these nodules increase the resistance to portal blood flow, which can lead to portal hypertension. […] Esophageal variceal bleeding is a complication of portal hypertension and a major cause of death in patients with liver cirrhosis. Combined treatment with vasoactive drugs, prophylactic antibiotics, and endoscopic band ligation is the standard of care for patients with acute bleeding. However, this treatment fails in about 10% to 15% of these patients. A TIPS creates a connection between the portal and hepatic veins, resulting in portal decompression and homeostasis. […] A TIPS remains the only choice to control acute variceal bleeding refractory to medical and endoscopic therapy, with a success rate of 90% to 100%. The urgency of TIPS placement is an independent predictor of early mortality.

• #36

  https://journals.lww.com/md-journal/fulltext/2020/01310/propranolol_plus_endoscopic_ligation_for_variceal.44.aspx

  The use of NSBB might worsen the prognosis of cirrhotic patients with significant ascites. These results suggest that EVL alone is a more appropriate treatment option for prophylaxis of esophageal varices than propranolol combination therapy when patients have significant ascites. […] In patients with cirrhosis and esophageal varices, the incidence of variceal bleeding is about 12% to 15% per year. Mortality rate due to bleeding is still high up to 20%. Mortality of variceal bleeding is usually determined by size of varices or basal liver function. […] NSBB has both hemodynamic and non-hemodynamic effects. It hemodynamically reduces the portal inflow. It also directly decreases the variceal flow, thus reducing variceal growth and blocking the occurrence of collateral circulation. […] There is a continuing concern about the safety of NSBB use first raised from the window hypothesis. Recently, it has been reported that when using NSBB for 6 months in a patient with Child-Pugh class C, MELD 18 points or more, or ascites, OS is decreased from 15 months to 11 months.

• #37 Bleeding esophageal varices: Who should receive a shunt? | Cleveland Clinic Journal of Medicine

  https://www.ccjm.org/content/84/3/199

  Once varices bleed, the risk of rebleeding is higher than 50%, and rebleeding is associated with a high mortality rate. TIPS should be considered if nonselective beta-blockers and surveillance with upper endoscopy and banding fail to prevent rebleeding, with many studies showing a TIPS to be superior to pharmacologic and endoscopic therapies. […] The authors concluded that early use of TIPS in patients with cirrhosis and Child-Pugh scores of 7 to 13 who were hospitalized for acute variceal bleeding was associated with significant reductions in rates of treatment failure and mortality.

• #38

  https://xiahepublishing.com/2310-8819/JCTH-2023-00061

  HVPG10 mmHg is a predictor of varicose vein formation and decompensation of liver cirrhosis, with HVPG20 mmHg indicating a poor prognosis. […] The diameter of the vessel is closely correlated with the tension of the vascular wall and the HVPG. […] Under the same intravascular pressure, the larger the diameter, the greater the tension of the vessel wall, and the more likely it is to rupture. […] The rate of late bleeding recurrence in patients without EVB prophylaxis is approximately 60%, most of which occurs within 12 years of the first bleeding. […] Child-Pugh class, albumin level, and international normalized ratio (INR) are associated with CSPH and can be used for risk assessment in patients with compensated and decompensated cirrhosis. […] Three criteria, including Child-Pugh class C, INR1.5, portal vein diameter 13 mm, and significant thrombocytopenia, can predict the possibility of varicose veins in patients with liver cirrhosis.

• #39

  https://xiahepublishing.com/2310-8819/JCTH-2023-00061

  Portal hypertension also promotes angiogenesis of hepatic vein branches and formation of portal-systemic collateral circulation, after which the dilation of splanchnic vessels leads to increased blood flow without reduction of intrahepatic resistance. […] Therefore, spontaneous portosystemic shunts are not effective for decompression and portal hypertension persists. […] The risk of developing liver decompensation and mortality in patients with GOV is significantly higher than in those without GOV. […] Overall, GOV can be detected in approximately 50% of patients with cirrhosis and is closely related to the severity of liver disease. […] HVPG is an effective method for assessing the risk of portal hypertension. […] Portal hypertension is defined as an HVPG of 5 mmHg (normal range, 3-5 mmHg).

• #40 Management of gastroesophageal varices in cirrhotic patients: current status and future directions | Annals of Hepatology

  https://www.elsevier.es/en-revista-annals-hepatology-16-articulo-management-gastroesophageal-varices-in-cirrhotic-S1665268119306507

  In medical practice, clinicians should determine the optimal treatment for GEV based on treatment situations and principles. Two possible treatment situations are primary prophylaxis for bleeding and emergent treatment for bleeding followed by secondary prophylaxis. […] Treatment principles can be classified into two categories: decreasing portal pressure and obstructing GEV. […] In 2007, the practice guidelines for management of GEV were endorsed by the American Association for the Study of Liver Diseases (AASLD) and the American College of Gastroenterology (ACG). […] Non-selective -blockers are recommended for patients with small varices that have an increased risk of bleeding, as with Child-Pugh class B/C cirrhosis or varices with red wale markings. […] The limitations of non-selective -blockers include possible non-responsiveness; contraindications for patients with asthma, insulin-dependent diabetes, or peripheral vascular disease; and limited tolerability due to adverse effects, such as general fatigue and lightheadedness.

• #41 Clinical and Molecular Hepatology

  https://www.e-cmh.org/m/journal/view.php?number=1394

  Because the splanchnic vasodilatation is the main step in the development and progression of portal hypertension, drugs which can lead splanchnic vasoconstriction, such as nonselective betablockers (NSBBs), terlipressin, somatostatin, and its analogues (octreotide, vapreotide) reduce portal pressure and, currently, these drugs are widely used in the management of GEVs. […] Various studies suggested that NSBBs is effective in the prevention of bleeding from EVs and recent practice guidelines recommend use of NSBBs for reducing portal pressure, leading to primary and secondary prophylaxis against variceal bleeding in patients with cirrhosis and high-risk EVs. […] The optimal dose is 12.5 mg once a day because higher doses have no additional benefit in HVPG with higher reduction of arterial pressure.

• #42 Varices – Gastrointestinal Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/gastrointestinal-disorders/gastrointestinal-bleeding/varices

  Varices are dilated veins in the distal esophagus or proximal stomach caused by elevated pressure in the portal venous system, typically from cirrhosis. […] The most dangerous collaterals occur in the distal esophagus and gastric fundus, causing engorged, serpentine submucosal vessels known as varices. These varices partially decompress portal hypertension but can rupture, causing massive gastrointestinal (GI) bleeding. […] Because varices are diagnosed only during endoscopy, the primary treatment is endoscopic. Endoscopic banding of varices is preferred over injection sclerotherapy. […] Octreotide increases splanchnic vascular resistance by inhibiting the release of splanchnic vasodilator hormones (eg, glucagon, vasoactive intestinal peptide). […] If bleeding continues or recurs despite these measures, emergency techniques to shunt blood from the portal system to the vena cava can lower portal pressure and diminish bleeding. A TIPS procedure is the emergency intervention of choice. […] Liver transplantation can also decompress the portal system but is a practical option only for patients already on a transplant list. […] The severity of the underlying liver disease is a major determinant of mortality of a bleeding episode.

• #43 Clinical and Molecular Hepatology

  https://www.e-cmh.org/m/journal/view.php?number=1394

  Although several studies evaluated the efficacy of carvedilol in the primary and secondary prophylaxis against variceal bleeding, results are conflicting. […] However, recurrence rate after EBL is significantly higher than after EIS, although both procedures are local therapies. […] In EBL, the effect of EBL effect is usually limited to the mucosa and submucosa, while perforating veins between the paraesophageal veins and submucosal veins are preserved. […] The major disadvantage after TIPS procedure is variceal rebleeding caused by obliteration or stenosis of shunt. […] To prevent rebleeding of varices, hepatic venous pressure gradient should be controlled lower than 12 mmHg. […] Because development of GEVs is a direct consequence of portal hypertension, reduction of portal pressure by NSBBs from the early stage of liver cirrhosis might ameliorate the development of GEVs.

• #44 What are esophageal varices? Types, treatments, and more

  https://www.medicalnewstoday.com/articles/esophageal-varices

  Endoscopic sclerotherapy involves using an endoscope to perform minor medical tasks, such as injecting a medication into the swollen veins to make them shrink. […] Endoscopic variceal banding involves using the same tool to place a rubber band around a varice to prevent the vessel from bleeding. […] A doctor may recommend a transjugular intrahepatic portosystemic shunt, or TIPS, procedure. This involves using an X-ray to guide the placement of a small tube to connect the portal vein with the hepatic vein. This creates a new channel for blood, reducing pressure in the portal vein. […] Esophageal varices usually result from cirrhosis and portal hypertension.

• #45 Beta blockers in portal hypertension. Are they really a good option? | Annals of Hepatology

  https://www.elsevier.es/en-revista-annals-hepatology-16-articulo-beta-blockers-in-portal-hypertension–S166526811932023X

  Derivative surgery has been used for over 50 years in secondary prophylaxis. It is based on shunting the blood flow from the portal territory. It is a useful alternative for reducing re-bleeding risk, but with the disadvantage of increasing encephalopathy and hepatic failure in non-selective techniques. […] TIPS result in very controlled shunting with respect to diameter. Additionally, a surgical procedure is not necessary; thus, related morbimortality is very low. Nevertheless, results are not encouraging due to the dysfunction rate of more than 50% in the first year due to proliferation of the intimae into the shunt.

Zobacz więcej