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Nonselective β-blocker therapy and endoscopic variceal ligation reduce the incidence of variceal hemorrhage in cirrhotic adults, but their use in children is controversial. There are no evidence-based recommendations for the prophylactic management of children at risk of variceal hemorrhage due to the lack of appropriate randomized controlled trials. In a recent gathering of experts at the American Association for the Study of Liver Diseases annual meeting, significant challenges were identified in attempting to design and implement a clinical trial of primary prophylaxis in children using either of these therapies. These challenges render such a trial unfeasible, primarily due to the large sample size required, inadequate knowledge of appropriate dosing of β-blockers, and difficulty in recruiting to a trial of endoscopic variceal ligation. Pediatric research should focus on addressing questions of natural history and diagnosis of varices, prediction of variceal bleeding, optimal approaches to β-blocker and ligation therapy, and alternative study designs to explore therapeutic efficacy in children.

Purpose of Review: Report on significant advances in the pathophysiology, diagnosis, and management of the complications of portal hypertension that have occurred in the last year., Recent Findings: The specific areas reviewed refer to experimental studies aimed at modifying the factors that lead to portal hypertension (increased intrahepatic vascular resistance and splanchnic vasodilatation) and recent advances in the diagnosis and management of the complications of portal hypertension. The specific complications reviewed in this paper are varices and variceal bleeding (primary prophylaxis, treatment of the acute episode, and secondary prophylaxis), ascites and some of its complications (hyponatremia, hepatic hydrothorax), hepatorenal syndrome, spontaneous bacterial peritonitis, and hepatic encephalopathy., Summary: Important studies, mostly prospective, regarding the management of the complications of portal hypertension are reviewed, including trials that demonstrate the value of the hepatic venous pressure gradient in predicting these complications, a trial of beta-blockers in patients with small varices, a randomized trial of transjugular intrahepatic portosystemic shunt using covered stents and another pilot study using this shunt in the treatment of hepatorenal syndrome, a trial of antibiotic prophylaxis in preventing early variceal rebleeding, and a trial of synbiotic therapy in hepatic encephalopathy. These trials will contribute to advancing the practice of hepatology and defining future research areas.

Purpose of Review: This review discusses the advances in the pathophysiology, diagnosis, and management of the complications of portal hypertension that have occurred in the past year., Recent Findings: The specific topics reviewed are the pathophysiology of portal hypertension (including recent findings regarding intrahepatic vascular resistance and splanchnic vasodilatation) and experimental methods used to act on the mechanisms that lead to portal hypertension, as well as recent advances in the diagnosis and management of the complications of portal hypertension., Summary: The specific complications discussed in this review are varices and variceal bleeding (primary prophylaxis, treatment of the acute episode, and secondary prophylaxis), portal hypertensive gastropathy, ascites, hepatorenal syndrome, spontaneous bacterial peritonitis, the cardiopulmonary complications of portal hypertension (hepatopulmonary syndrome, portopulmonary hypertension, cardiac dysfunction), and hepatic encephalopathy.

Portal hypertension, the main complication of cirrhosis, is responsible for its most common complications: variceal hemorrhage, ascites, and portosystemic encephalopathy. Portal hypertension is the result of increased intrahepatic resistance and increased portal venous inflow. Vasodilatation (splanchnic and systemic) and the hyperdynamic circulation are hemodynamic abnormalities typical of cirrhosis and portal hypertension. Gastroesophageal varices result almost solely from portal hypertension, although the hyperdynamic circulation contributes to variceal growth and hemorrhage. Ascites results from sinusoidal hypertension and sodium retention, which, in turn, is secondary to vasodilatation and activation of neurohumoral systems. The hepatorenal syndrome represents the result of extreme vasodilatation, with an extreme decrease in effective blood volume that leads to maximal activation of vasoconstrictive systems, renal vasoconstriction, and renal failure. Spontaneous bacterial peritonitis is a potentially lethal infection of ascites that occurs in the absence of a local source of infection. Portosystemic encephalopathy is a consequence of both portal hypertension (shunting of blood through portosystemic collaterals) and hepatic insufficiency that result in the accumulation of neurotoxins in the brain. This review covers the recent advances in the pathophysiology and management of the complications of portal hypertension.

Portal hypertension is the main complication of cirrhosis and is responsible for its most common complications: variceal hemorrhage, ascites, and portosystemic encephalopathy. Portal hypertension is the result of increased intrahepatic resistance and increased portal venous inflow. Vasodilatation (splanchnic and systemic) and the hyperdynamic circulation are hemodynamic abnormalities typical of cirrhosis and portal hypertension. Gastroesophageal varices result almost solely from portal hypertension, although the hyperdynamic circulation contributes to variceal growth and hemorrhage. Ascites results from sinusoidal hypertension and sodium retention, which is in turn secondary to vasodilatation and activation of neurohumoral systems. Hepatic hydrothorax results from the passage of ascites across the diaphragm and into the pleural space. The hepatorenal syndrome represents the result of extreme vasodilatation with an extreme decrease in effective blood volume that leads to maximal activation of vasoconstrictive systems, renal vasoconstriction, and renal failure. Spontaneous bacterial peritonitis is a potentially lethal infection of ascites that occurs in the absence of a local source of infection. Portosystemic encephalopathy is a consequence of both portal hypertension (shunting of blood through portosystemic collaterals) and hepatic insufficiency resulting in the accumulation of neurotoxins in the brain.

Cirrhosis represents the end stage of any chronic liver disease. Two major syndromes result from cirrhosis: portal hypertension and hepatic insufficiency. Additionally, vasodilatation and the hyperdynamic circulation are hemodynamic abnormalities typical of cirrhosis and portal hypertension. Complications of cirrhosis occur as a consequence of a combination of these factors. Gastroesophageal varices result almost solely from portal hypertension, although the hyperdynamic circulation contributes to variceal growth and hemorrhage. Ascites results from sinusoidal hypertension and sodium retention, which is, in turn, secondary to vasodilatation and activation of neurohumoral systems. Hyponatremia and the hepatorenal syndrome result from water retention and renal vasoconstriction, respectively, both of which are also consequences of peripheral vasodilatation. Vasodilatation that occurs in the pulmonary circulation leads to the hepatopulmonary syndrome. Another complication of cirrhosis, portosystemic encephalopathy, is a consequence of both portal hypertension (shunting of blood through portosystemic collaterals) and hepatic insufficiency. This paper reviews the recent advances in the pathophysiology and management of the complications of cirrhosis and portal hypertension.