What is the mechanism by which ammonia accumulates in cases of hepatic coma?

Ammonia accumulates in cases of hepatic coma primarily through increased production from bacterial metabolism in the intestines. In individuals with liver dysfunction, the liver's ability to detoxify ammonia is significantly impaired. Normally, the liver converts ammonia, which is a byproduct of protein metabolism, into urea for excretion via the kidneys. However, in hepatic coma, this detoxification pathway is disrupted.

When the liver's function declines, especially in conditions such as cirrhosis or acute liver failure, there is a rise in ammonia levels in the bloodstream. One primary source of ammonia production is the gut, where bacteria break down proteins into amino acids and produce ammonia as a metabolic byproduct. In a healthy individual, much of this intestinally produced ammonia would be captured and converted to urea in the liver. However, in patients with liver failure, the compromised liver cannot handle the increased load of ammonia from intestinal bacteria effectively, leading to its accumulation.

This mechanism of ammonia production accentuates the risk of hepatic encephalopathy, a condition characterized by confusion, altered level of consciousness, and potentially coma due to the toxic effects of elevated ammonia on the brain. Understanding this process highlights the importance of managing risk factors associated with bacterial overgrowth and protein intake