Managing Upper GI Bleeding Due to Portal Hypertension

Rowen K. Zetterman, MD


April 27, 2017

In This Article

New Guidance for Portal Hypertension

The American Association for the Study of Liver Diseases recently published practice guidance for evaluation, diagnosis, and treatment of upper gastrointestinal bleeding as a consequence of portal hypertension (PH).[1] They note in their introduction that practice guidance is distinct from a practice guideline in that it provides guidance statements, not recommendations. They note that "guidance provides a data-supported approach" and that "it is not intended to replace clinical judgment, but rather to provide general guidance applicable to the majority of patients."

Cirrhosis and Portal Hypertension

Cirrhosis results from chronic liver injury due to a host of factors. Hepatitis B virus (HBV), hepatitis C virus (HCV), excessive alcohol consumption, and nonalcoholic fatty liver disease account for the majority of cases in the United States.[2]

The progressive development of hepatic fibrosis and regenerative nodule formation results in disruption and resistance to blood flow in the portal circulation and hepatic sinusoids, causing PH. Thus, many of the causes of cirrhosis and prevention of PH can be ameliorated by control of the dominant risk factor (eg, cessation of excessive alcohol consumption and reduction of obesity) or by pharmacologic treatments (eg, HBV and HCV therapeutic agents).


  • "Elimination of the etiologic agent is the current mainstay of therapy" to prevent development of cirrhosis and resulting portal hypertension.

Clinical Manifestations of Portal Hypertension

The initial phase of cirrhosis may be "compensated" and characterized by lack of observable clinical manifestations of end-stage disease, such as ascites, encephalopathy, or bleeding esophageal varices (EV).[3] Patients with compensated cirrhosis (CC) may be asymptomatic and not even recognize their underlying illness. CC represents a slowly progressive stage of liver injury, with a low 5-year mortality.[4]

The development of PH accounts for most liver-related complications of end-stage liver disease.[1] Portal hypertension can be present in compensated patients lacking ascites, or encephalopathy[5] and asymptomatic gastroesophageal varices (GEV) can be present. Patients with clinically significant portal hypertension (CSPH) have a greater likelihood of developing GEV and other signs of clinical decompensation.[6] A case can be made that upper endoscopy should be completed in all patients with CC, because patient prognosis is worse when varices are present.[7]

Decompensated cirrhosis is defined by the clinical findings of ascites, encephalopathy, variceal bleeding, and/or worsening hepatic function. Manifestations of decompensation may occur alone or in combination. Ascites is often the first manifestation of PH to present.[8] Gastroesophageal varices are frequently present in patients with decompensated cirrhosis, and upper endoscopy should be undertaken if not done previously. Decompensation of patients with cirrhosis is a predictor of variceal progression.[5]

Bleeding from varices can be the initial sign of decompensation. The combination of bleeding GEV plus other manifestations of decompensation, such as ascites and encephalopathy, has a much worse prognosis than isolated variceal hemorrhage (VH).[4] Decompensation may also develop with systemic infection.[9]

Once a person is initially hospitalized for decompensated cirrhosis, 25% will require rehospitalization within 30 days owing to clinical worsening.[3] Decompensated cirrhosis may be complicated by acute-on-chronic liver failure[10] that can follow such events as systemic infection, exacerbation of alcoholic hepatitis, or HBV reactivation. Systemic inflammation is invariably present in acute-on-chronic liver failure associated with multiorgan failure and increased 30-day mortality.


  • Cirrhosis should be described, analyzed, and managed in two distinct clinical stages, compensated and decompensated...

  • ...[C]ompensated cirrhosis should be substaged into those with mild PH and those with CSPH...

  • Patients with CSPH are substaged into those with and without GEV.


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