Purpose of review
To evaluate the significance of blood lactate increase during enteral nutrition in the critically ill, and to propose diagnostic and therapeutic strategies.
Recent findings
Acute mesenteric ischemia occurs in approximately 1% of critically ill patients treated with catecholamine. Recent literature suggests that enteral nutrition is a risk factor of acute mesenteric ischemia, in particular in case of low cardiac output, by a mechanism of nonocclusive mesenteric ischemia. The association of clinical, biological, and computed tomography imaging might help to evaluate the reversibility of acute mesenteric ischemia.
Summary
As enteral nutrition induces an increased metabolic work of the gut, the inadequation between oxygen delivery and demand exposes the gut to a phenomenon of nonocclusive mesenteric ischemia. Before initiation of enteral nutrition,, and before each increase of the enteral nutrition dose, the risk factors of nonocclusive mesenteric ischemia should be searched in order to prevent it. While under enteral nutrition, increased lactate concentration while receiving enteral nutrition requires the urgent search for nonocclusive mesenteric ischemia, and the adaptation of enteral nutrition (reduction, stop, and/or switch to parenteral nutrition or tolerate early nutrient restriction). Early signs of nonocclusive mesenteric ischemia should be searched in order to allow for a rapid diagnosis, before development of irreversible transmural necrosis. After the diagnosis of acute mesenteric ischemia, improving the balance between oxygen demand and delivery to the gut, evaluating the reversibility of the gut ischemia, and performing urgent resection in case of irreversible transmural necrosis should be the main objectives. After the resolution of acute mesenteric ischemia, the benefit risk analysis of enteral nutrition reintroduction should be evaluated.
