Newer aspects of hepatic encephalopathy.

Recently attempts have been made to standardize terminology in the field of hepatic encephalopathy. We are now facing a new problem. Chronic hepatitis C-induced cirrhosis occurs in an older population; this may change the presentation pattern of hepatic encephalopathy in future. Ammonia has once again become prominent as the leading toxin likely to play a role in the pathogenesis of this syndrome. How ammonia interacts with other proposed mechanisms should be an area of active research. The treatment arena has seen some advances. Unfortunately, the economics of having newer treatments approved in the USA is formidable. Rifaximine, L-ornithine-L-aspartate, sodium benzoate and possibly flumazenil appear to be significant advances. More elective shunt suppression for selected patients will be seen. Liver transplantation remains the only option for truly intractable hepatic encephalopathy.

Interplay of portal pressure, portal perfusion and hepatic arterial inflow in modulating expression of hepatic encephalopathy in patients with spontaneous or artificially created portosystemic shunts.

The major theme of this discussion is how portal pressure after portosystemic shunt procedures may modulate the expression of hepatic encephalopathy. Decades of emphasis on the paramount importance of maintaining portal venous perfusion after shunt procedures is now being re-examined. In countries where non-cirrhotic portal hypertension is common, physicians have long recognized that hepatic encephalopathy is rare even with total portosystemic shunting. However, once decompressive shunts are created, hepatic encephalopathy becomes a clinical problem. Why this occurs needs to be better understood. In the meantime, there has been virtual abandonment of surgical shunts in favor of endoscopic variceal ablation treatment. This is despite the fact that surgical shunts that only partially decompress the portal hypertension are associated with excellent long-term control of variceal bleeding and low rates of hepatic encephalopathy. The time has come to once again examine the key relationship between portal pressure, portal perfusion with hepatic arterial inflow in inducing hepatic encephalopathy after creation of portosystemic shunts.