This explains the rationale for treating portal hypertension with a low-sodium diet and diuretics to attenuate the hyperkinetic state. Formation of varices An elevated pressure difference between systemic and portal circulation (ie, hvpg) directly contributes to the development of varices. 8, 12, 13 hvpg is a surrogate marker of portal pressure gradient and is derived from whvp corrected (subtracted) with free hepatic venous pressure (fhvp). The hypertensive portal vein is decompressed by diverting up to 90 of the portal flow through portasystemic 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). 8, 12, 13, 14 gastroesophageal varices have 2 main inflows. The first is the left gastric vein, and the second is the splenic hilum, through the short gastric veins.
A study in 230 patients with esophageal and/or gastric varices using portal vein catheterization. PubMed, google Scholar. Chao y, lin hc, lee fy,. Hepatic hemodynamic features in patients with esophageal or gastric varices. Gastric varices: is there a role for endoscopic cyanoacrylates, or are we entering the brto era? Kravetz d, sikuler e, groszmann. Splanchnic and systemic hemodynamics in portal hypertensive rats during hemorrhage and blood volume restitution. PubMed google Scholar. Castaneda b, morales j, lionetti r,.
Excessive doses of vitamin A taken for months or years can lead to chronic hepatic disease. Intake of doses ranging from as small as 3-fold the recommended daily dose continued for several years to doses as high as 20-fold the approved dose for a few months can lead to hepatic disease. The pericellular fibrosis characteristic of vitamin A toxicity may lead to portal hypertension. Postsinusoidal obstruction syndrome and veno-occlusive disease of the liver are postsinusoidal causes of resistance. Posthepatic resistance posthepatic causes of resistance to flow include the following: Thrombosis of the inferior vena cava (IVC) Right-sided heart failure constrictive pericarditis severe tricuspid regurgitation Budd-Chiari syndrome Arterial-portal venous fistula Increased portal blood flow Increased splenic flow Increase in portal blood flow The second. This increase is established through splanchnic arteriolar vasodilatation caused by an excessive release of endogenous vasodilators (eg, endothelial, neural, humoral). The increase in portal blood flow aggravates the increase in portal pressure; the increased flow contributes to the ability of portal hypertension to exist despite the formation of an extensive network of portosystemic collaterals that may divert as much as 80 of the portal blood. Manifestations of splanchnic vasodilatation include increased cardiac output, arterial hypotension, and hypervolemia.
Treatment of, gastric Varices - news Medical
Obstruction and increased resistance can occur at 3 levels in relation to the hepatic sinusoids, as follows (see the table, below Presinusoidal venous block (eg, portal vein thrombosis, schistosomiasis, primary biliary cirrhosis) - characterized by elevated portal venous pressure and a normal wedged hepatic venous. Postsinusoidal obstruction (eg, right sided heart failure, inferior vena caval obstruction) - whvp is characteristically elevated, whereas the hvpg and fhvp can be either elevated or normal, depending on the site of albany the obstruction (intrahepatic postsinusoidal vs posthepatic obstruction). Sinusoidal obstruction (eg, cirrhosis) - characterized by hvpg, fhvp, and whvp, with whvp being equal to portal venous pressure (because disrupted intersinusoidal communications diminishes compressibility and compliance of the sinusoids, allowing direct transmission of portal pressure to the whvp). Interpretation of Surrogate portal Venous Pressure measurements in the differential diagnosis of Portal Hypertension (Open Table in a new window). Etiology of Portal Hypertension, whvp, fhvp, hVPG.
Prehepatic, normal, normal, normal, intrahepatic, presinusoidal, normal, normal, normal, sinusoidal, increased, increased, increased, postsinusoidal, increased, normal Increased Posthepatic Budd-Chiari syndrome N/a hepatic vein cannot be cannulated N/A Other posthepatic causes Increased Increased Normal fhvp free hepatic venous pressure; hvpg hepatic venous pressure gradient; N/A not. With regard to the liver itself, causes of portal hypertension usually are classified as prehepatic, intrahepatic, and posthepatic. Prehepatic resistance Prehepatic causes of increased resistance to flow include the following: Portal vein thrombosis 10 Splenic vein thrombosis Congenital atresia or stenosis of portal vein Extrinsic compression (tumors) Splanchnic arteriovenous fistula Intrahepatic resistance Studies of hepatic microcirculation have identified several mechanisms that may explain. These mechanisms may be summarized benen as follows 6 : A reduction of sinusoidal caliber due to hepatocyte enlargement An alteration in the elastic properties of the sinusoidal wall due to collagen deposition in the space of Disse compression of hepatic venules by regeneration nodules Central. This probably is due to vascular injury.
In cirrhosis, the increase occurs at the hepatic microcirculation (sinusoidal portal hypertension). Increased hepatic vascular resistance in cirrhosis is not only a mechanical consequence of the hepatic architectural disorder; a dynamic component also exists due to the active contraction of myofibroblasts, activated stellate cells, and vascular smooth-muscle cells of the intrahepatic veins. Endogenous factors and pharmacologic agents that modify the dynamic component include those that increase or decrease hepatic vascular resistance. Factors that increase hepatic vascular resistance include endothelin-1 (ET-1 alpha-adrenergic stimulus, and angiotensin. Factors that decrease hepatic vascular resistance include nitric oxide (no 6 prostacyclin, and vasodilating drugs (eg, organic nitrates, adrenolytics, calcium channel blockers).
4, 7, endothelin and nitric oxide, studies have demonstrated the role of et-1 and no in the pathogenesis of portal hypertension and esophageal varices. 4, 7, et-1 is a powerful vasoconstrictor synthesized by sinusoidal endothelial cells that has been implicated in the increased hepatic vascular resistance of cirrhosis and in the development of liver fibrosis. No is a vasodilator substance that is also synthesized by the sinusoidal endothelial cells. In the cirrhotic liver, the production of no is decreased, and endothelial nitric oxide synthase (enos) activity and nitrite production by sinusoidal endothelial cells are reduced. As a result, intrahepatic vasoconstriction occurs in cirrhotic liver and accounts for approximately 20-30 of the increased intrahepatic resistance. 7, 8, 9, another major contribution to the increased portal venous pressure is the concomitant splanchnic arteriolar vasodilation causing increased portal venous inflow. Location of resistance in relation to the liver and sinusoids.
Management of acute gastric varices bleeding - scienceDirect
Increase in vascular resistance, the initial factor in the etiology of portal hypertension is an increase in the vascular resistance to the portal blood flow. Poiseuilles law, which can be applied to portal vascular resistance, r, states that r 8hL/pr4, where h is the viscosity of blood, l is the length of the blood vessel, and r is the radius of the blood vessel. The viscosity of the blood is related to the hematocrit. The lengths of the blood vessels in the portal vasculature are relatively constant. Thus, changes in portal vascular resistance are determined primarily by blood vessel radius. Because bij portal vascular resistance is indirectly proportional to the fourth power of the vessel radius, small decreases in the vessel radius cause large increases in portal vascular resistance and, therefore, in portal blood pressure (p f8hL/pr4, verbranding where p is portal pressure and f is portal. Liver disease that decreases the portal vascular radius produces a dramatic increase in the portal vascular resistance.
kokawa h,. Risk factors for hemorrhage from gastric fundal varices. Watanabe k, kimura k, matsutani s,. Portal hemodynamics in patients with gastric varices.
Keywords, gastric varices Gastric variceal bleeding Endoscopic band ligation Sclerotherapy Cyanoacrylate injection EUS Transjugular intrahepatic van portosystemic shunt Balloon-occluded retrograde transvenous obliteration. Supplementary material, video.1, endoscopic band ligation for bleeding gastroesophageal varices type 1 (GOV1) (MP4 22524 kb). Video.2, technique of 2-octyl cyanoacrylate injection for fundal varices with stigmata of recent bleeding (MP4 21226 kb). Video.3, actively bleeding fundal varix treated with cyanoacrylate injection (MP4 7390 kb). Video.4, animation of balloon-occluded retrograde transvenous obliteration (brto) procedure for treatment of gastric varices (MP4 6488 kb). Sarin sk, lahoti d, saxena sp,. Prevalence, classification and natural history of gastric varices: a long-term follow-up study in 568 portal hypertension patients.
Gastric Variceal Bleeding in the Elderly - scienceDirect
Chapter 632 Downloads, abstract, gastric variceal hemorrhage is one of the how most dreaded endoscopic emergencies. Optimal management recommendations are limited by the lack of robust evidence-based data. Although endoscopic band ligation and sclerotherapy are effective modalities for esophageal variceal bleeding, they are suboptimal therapies for fundal variceal hemorrhage. Endoscopic cyanoacrylate injection is considered a first-line treatment option, where available. The role of eus-guided angiotherapy for gastric variceal bleeding is promising. Non-endoscopic treatment options include transjugular intrahepatic portosystemic shunt and balloon-occluded retrograde transvenous obliteration. There is a need for prospective comparative studies among the various treatment modalities to further define optimal management algorithms for gastric variceal hemorrhage. This chapter includes supplementary videos.