Splanchnic metabolism in acute liver failure and sepsis

A number of papers have suggested that the splanchnic circulation and oxidative metabolism are compromised in critical illness. This review discusses this hypothesis and outlines the recent advances in the understanding of splanchnic metabolism with special focus on acute liver failure and hyperdynamic sepsis.

Splanchnic blood flow, oxygen delivery, and consumption are increased in both acute liver failure and sepsis. The capability of the liver to extract oxygen, even under extreme conditions, renders the liver less prone to hypoxia. A common feature of acute liver failure and sepsis is a hypermetabolic state with enhanced glycolysis and production of lactate and pyruvate. Human studies on other features of intermediary metabolism are sparse, but there are indications that several intermediary processes are severely compromised in patients with acute liver failure, whereas these processes are maintained in sepsis.

There is increasing evidence that both acute liver failure and sepsis are accompanied by a hypermetabolic state in the hepatosplanchnic area, characterized by enhanced glycolysis and hyperlactatemia. This should not be rigorously interpreted as an indication of hypoxia. In fact, clinically important splanchnic hypoxia may be a relatively uncommon phenomenon in such patients.