BILIARY TRACT: CLINICAL REVIEW
Management of Portal Hypertension
Hubert H. Nietsch, MD
Abstract: Complications of portal hypertension are the leading
cause of death in patients with liver cirrhosis. Rational medical and endoscopic therapy is guided by a thorough understanding of the underlying pathophysiology of ascites, variceal formation and bleeding,hepatorenal syndrome, and hepatic encephalopathy. The pathophysiology of each clinical entity is reviewed followed by an evidence-based diagnostic and management algorithm. Key Words: portal hypertension, varices, ascites, hepatorenal syndrome, management (J Clin Gastroenterol 2005;39:232–236)
portal system mediated by arteriolar vasodilation and hence aggravates portal hypertension.6
VaricealBleeding and Management
The most life-threatening complication of portal hypertension is acute variceal bleeding with a mortality as high as 30% depending on the stage of liver disease.7 Varices are either isolated at the gastroesophageal junction or communicate with fundal veins leading to gastric varices. The risk of bleeding correlates strongly with portal pressures and varices generally do notbleed unless portal pressures are .12 mmHg, which serves as a target pressure to reduce portal hypertension.8 The risk of venous wall rupture correlates with wall tension described by Laplace’s law, wherein tension is deﬁned by the product of the intraluminal to extraluminal pressure gradient (Pi 2 Pe) and the vessel radius (r) divided by the wall thickness (w) (T = (Pi 2 Pe) 3 r/w). Endoscopicassessment of risk of variceal bleeding depends on variceal size and signs of wall thinning (hematocystic spots, red wale sign).9,10 De novo variceal formation is estimated at about 6%/year in compensated cirrhosis.7 Annual endoscopies for variceal screening are therefore still recommended but might not be cost-effective.11 Treatment strategies for portal hypertension can be divided in threecategories: primary prevention of bleeding, secondary prevention after a previous bleeding episode, and management of acute hemorrhage.
ortal hypertension with its complications is the leading cause of death in patients with liver cirrhosis. The severity of portal hypertension correlates strongly with overall patient survival.1 This review will focus on the pathophysiology of portal hypertension and themanagement of esophageal varices, ascites, hepatorenal syndrome, and hepatic encephalopathy.
Normal pressures in the human portal venous system range from 3 to 6 mmHg. Portal hypertension is deﬁned by an increase above 10 mmHg. Pressure changes in the portal system follow Ohm’s law (DP = Q 3 R), where pressure (P) is deﬁned as the product of ﬂow (Q) and resistance (R).2This simple equation provides the rationale to the two main strategies of therapeutically lowering portal pressures by either decreasing portal inﬂow or reducing the sinusoidal resistance or a combination of both. The increased resistance is caused by prehepatic or posthepatic obstruction of blood ﬂow; in most of cases of portal hypertension, resistance is secondary to intrahepatic causes due toliver cirrhosis mediated by an increase in sinusoidal pressures.3 Increased vascular resistance in such cases consists of a ﬁxed and dynamic component caused by liver ﬁbrosis and vasospasm, respectively. The vasospastic component is mediated by endothelin,4 angiotensin, and other factors. Simultaneously vasodilating factors such as nitric oxide (NO) are decreased in the hepatic circulation leading toan imbalance between vasoconstrictor and vasodilator stimuli.5 This results in endothelial dysfunction of the hepatic microcirculation and increases splanchnic blood ﬂow into the
Acute Variceal Bleeding
The management of acute bleeding requires a multidisciplinary approach. The patient should be admitted to an intensive care unit, where appropriate resuscitation can be performed. It is of...