AASLD Practice Guidance on risk stratification and management of portal hypertension and varices in cirrhosis

Abstract

Portal hypertension results from a series of maladaptive responses to chronic liver injury and cirrhosis. Initially, structural mechanisms because of accumulation of fibrous tissue, regenerative nodules, microthrombi, parenchymal extinction, and collapse lead to an increase in intrahepatic vascular resistance (1). In addition to architectural distortion, dynamic sinusoidal vasoconstriction contributes to 30% of the total increase in vascular tone. These structural changes lead to an increased portal pressure gradient; when this reaches values of about 10 mm Hg, it gives rise to formation of portal-systemic collaterals and compensatory splanchnic vasodilation, which, in turn, increases portal blood flow and, consequently, portal pressure (2). One of the first consequences of portal hypertension is the development of portosystemic collaterals, for which vascular endothelial growth factor (VEGF)-driven angiogenesis plays an important role (3). Gastroesophageal varices represent the most clinically relevant collaterals because of their increased risk of bleeding. Bleeding is directly dependent on increased wall tension at the varices, determined by portal pressure, variceal diameter, and thin wall thickness. Vasodilation occurs also in the systemic circulation resulting in a hyperdynamic circulatory state, driven by decreased effective arterial blood volume leading to activation of neurohumoral and vasoconstrictive systems, sodium and water retention, and increased cardiac output. This process eventually results in the development of ascites and, at late stages, hepatorenal syndrome because of compensatory renal vasoconstriction. Hepatic encephalopathy represents a multifactorial complication of portal hypertension, resulting from portosystemic shunting, impaired synthetic liver function, increased bacterial translocation, and muscle wasting (sarcopenia). Finally, imbalances on vasoconstrictors and vasodilators in the pulmonary circulation results in hepatopulmonary syndrome (increased vasodilation) and portopulmonary hypertension (increased vasoconstriction). CO, carbon monoxide; H 2 S, hydrogen sulfide; HVR, hepatic vascular resistance; NO, nitric oxide; ET, endothelin.

Novel serum biomarker of Golgi protein 73 for the diagnosis of clinically significant portal hypertension in patients with compensated cirrhosis

“…This implies its potential role for drug evaluation in chronic liver disease. In patients with compensated cirrhosis combined with CSPH, nonselective beta‐blockers (NSBBs) are recommended for the treatment of CSPH 1 . Therefore, it is intriguing to further evaluate GP73 for therapeutic monitoring of NSBBs in patients with compensated cirrhosis with CSPH in the future.…”

AASLD Practice Guidance on the use of TIPS, variceal embolization, and retrograde transvenous obliteration in the management of variceal hemorrhage

“…Gastric varices can be grouped based on their endoscopic location as (1) gastroesophageal varices type 1 (GOV1): lesser curvature, (2) gastroesophageal varices type 2 (GOV2): greater curvature, (3) isolated gastric varices type 1: gastric fundus (IGV1), and (4) isolated gastric varices type 2: any location in the stomach other than the gastric fundus (IGV2). [9] Gastric varices are supplied by the left gastric vein (feeds GOV1, GOV2), or short gastric veins, and posterior gastric vein (feed IGV1, IGV2, GOV2) (Fig.…”

“…General management of bleeding from gastrofundal varices is the same as that for esophageal variceal hemorrhage, as specified in the AASLD guidance on portal hypertension. [1] In cases of massive bleeding, balloon tamponade (with Linton-Nachlas tube or Sengstaken-Blakemore tube with gastric balloon inflation) may serve as a bridge to other treatments. Endoscopy is performed for initial diagnosis of the source of bleeding.…”

“…Further treatment of esophageal varices should follow current applicable Guidelines. [1] Finally, because RTO has the potential to increase portal pressure with ensuing complications, treatment with NSBBs could be considered in patients with high-risk esophageal varices without contraindications.…”

“…

This is a comprehensive guidance on the use of interventional radiology endovascular techniques in the management of variceal hemorrhage from the American Association for the Study of Liver Diseases (AASLD). This guidance document is complementary to the AASLD "Risk Stratification and Management of Portal Hypertension and Varices in Cirrhosis" guidance [1] and addresses the recent advancements in these invasive procedures. Although the use of TIPS dates back to the 1980s, several new technical refinements in TIPS stents have occurred in the last few years.

…”