Reply to: 'encephalopathy or hepatic encephalopathy?': Management of critically-ill cirrhotic patients

摘要

In response to Montagnese et al. [1], we fully agree that hepatic encephalopathy is a multifactorial syndrome which may result from impaired liver function, portosystemic shunts as well as from non-hepatic factors including sepsis, electrolyte imbalance, and sedative agents. None of the manifestations of hepatic encephalopathy are specific to any of the mechanisms involved. Although we do not clearly understand what a "statistical definition" means in this context, we also agree that, as it is multifactorial and non-specific, "hepatic encephalopathy" might be better termed as "encephalopathy" in critically-ill cirrhotic patients who frequently have several precipitating factors. Elevated blood ammonia levels are the hallmark of encephalopathy in cirrhosis. However, the correlation between blood ammonia and severity of encephalopathy is weak [2]. In addition, due to a marked impairment in liver function, any critically-ill cirrhotic patient is expected to have elevated blood ammonia levels, whatever the severity of encephalopathy. Practically, the findings of elevated blood ammonia levels in this population may not exclude the contribution of non-hepatic factors in the occurrence of neuro-psychiatric changes. This is the reason why, in line with others [3], we have suggested that the systematic determination of blood ammonia levels is unlikely to be useful in the management of critically-ill cirrhotic patients [4].