Several causes of UGIB are the result of portal hypertension, including esophageal varices, PHG, gastric varices, and ectopic varices. However, it should be kept in mind that patients with portal hypertension can develop UGIB from sources unrelated to portal hypertension.
Varices (picture 3A-B and picture 4) develop as a consequence of portal hypertension in approximately 50 percent of patients with cirrhosis, and variceal hemorrhage occurs at an annual rate of 5 to 15 percent . The onset of UGIB from varices usually signifies significant portal hypertension, which is typically associated with advanced liver disease (Child-Pugh class B or C). Patients who develop bleeding while being treated with a beta blocker have a poor prognosis . The clinical presentation of patients with varices, which most commonly manifests as hematemesis and/or melena, may be similar to that seen in patients with bleeding from nonvariceal lesions . Indeed, differentiating variceal from nonvariceal bleeding based on clinical grounds, even in patients with known cirrhosis, is often difficult if not impossible.
Hepatic encephalopathy or portosystemic encephalopathy is a syndrome of largely reversible impairment of brain function occurring in patients with acute or chronic liver failure or when the liver is bypassed by portosystemic shunts. This leads to a spectrum of neurological impairments ranging from subclinical brain dysfunction to coma. The mechanisms causing this brain dysfunction are still largely unclear.
The liver has a central detoxifying role in the body with its capability of neutralizing many toxic chemicals absorbed from the gastrointestinal (GI) tract and others produced as byproducts of normal metabolism. Most of these toxins reach the liver through the portal venous system and going through the low flow hepatic sinusoids these substances are effectively captured and detoxified by hepatocytes. With the progression of liver fibrosis and development of cirrhosis the increased hepatic resistance forces the blood to bypass the liver by flowing through portosystemic shunts. This results in pooling of various toxins into the systemic circulation and eventually reaching the brain and other organs. In addition to these hemodynamic changes, the effective hepatocyte mass is significantly reduced in cirrhosis, thus it can be easily overwhelmed by relatively small amounts of toxins.
Normal brain function requires anatomical brain integrity, sufficient energy production, and efficient synapse neurotransmission, all of which are impaired in HE. Although the mechanism of this impairment is not very clear, several factors and pathways interact together resulting in the central nervous system (CNS) dysfunction which manifests clinically as varying degrees of HE. Thank you.