The Main Mechanism Behind Hepatic Encephalopathy Triggered by Massive Hemorrhage in Cirrhosis

One of the primary mechanisms behind hepatic encephalopathy triggered by massive gastrointestinal bleeding in patients with cirrhosis is an increase in intestinal blood accumulation. The digestive tract is anatomically divided into the upper and lower gastrointestinal tracts. In cases of significant upper gastrointestinal bleeding, blood enters the digestive system and becomes subject to digestion. Since blood contains a high concentration of plasma proteins, excessive bleeding can lead to increased protein metabolism and subsequent elevation in ammonia production within the gut.

Patients with cirrhosis already have impaired liver function, which significantly reduces their ability to metabolize ammonia. Additionally, when portosystemic shunting is present, ammonia produced in the intestines bypasses the liver and directly enters the systemic circulation, leading to elevated blood ammonia levels. Free ammonia is toxic and can cross the blood-brain barrier, affecting brain function in several key ways:

Ammonia disrupts the Krebs cycle in brain cells, impairing energy production and reducing the availability of energy to brain tissue.

Furthermore, ammonia increases the uptake of neutral amino acids such as tyrosine, phenylalanine, and tryptophan by the brain. These amino acids have an inhibitory effect on neurological function.

Another critical factor involves astrocytes in the brain, which contain glutamine synthetase. When ammonia levels rise, the production of glutamine increases significantly. Glutamine acts as a powerful intracellular osmotic agent, causing swelling not only in astrocytes but also in neurons. This cellular swelling plays a major role in the development of cerebral edema during hepatic encephalopathy.

Lastly, ammonia can directly interfere with neural electrical activity, further contributing to neurological dysfunction.

These interconnected processes represent crucial contributors to the onset and progression of hepatic encephalopathy following massive hemorrhage in cirrhotic patients.