Management of hepatic encephalopathy following transjugular intrahepatic portosystemic shunts: Current strategies and future directions

Figure 2 Metabolic profiles of blood ammonia in different populations. A: In the health, gut-derived ammonia is primarily metabolized in the liver via the urea cycle and excreted by the kidneys, maintaining blood ammonia as NH4⁺ and preventing its passage across the blood-brain barrier (BBB); B: In cirrhotic patients, impaired liver function disrupts the urea cycle, reducing ammonia conversion to urea. Combined with sarcopenia, which diminishes muscle ammonia metabolism, excess ammonia crosses the BBB, leading to astrocyte glutamine accumulation, swelling, and hepatic encephalopathy; C: In patients who undergo transjugular intrahepatic portosystemic shunt, sarcopenia may improve compared with non-transjugular intrahepatic portosystemic shunt patients; however, significant hepatic bypass of blood ammonia through the shunt leads to systemic circulation. This elevated ammonia can cross the BBB, increasing the risk of hepatic encephalopathy. Gln: Glutamine; GS: Glutamine synthetase; Glu: Glutamic acid.