Medical Intensive Care Unit, Besançon University Hospital, Besançon.
Medical Intensive Care Unit, Nantes University Hospital, Nantes.
Curr Opin Clin Nutr Metab Care. 2023 Mar 1;26(2):167-173. doi: 10.1097/MCO.0000000000000898. Epub 2022 Dec 23.
To evaluate the significance of blood lactate increase during enteral nutrition in the critically ill, and to propose diagnostic and therapeutic strategies.
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.
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.
评估危重病患者肠内营养时血乳酸升高的意义，并提出诊断和治疗策略。
接受儿茶酚胺治疗的危重病患者中，急性肠系膜缺血的发生率约为 1%。最近的文献表明，肠内营养是急性肠系膜缺血的一个危险因素，特别是在低心输出量的情况下，其机制是非闭塞性肠系膜缺血。临床、生物学和计算机断层成像的联合可能有助于评估急性肠系膜缺血的可逆性。
由于肠内营养会增加肠道的代谢工作量，而氧供与需求之间的不匹配会使肠道暴露于非闭塞性肠系膜缺血的现象中。在开始肠内营养之前，以及每次增加肠内营养剂量之前，都应该寻找非闭塞性肠系膜缺血的危险因素，以预防其发生。在接受肠内营养期间，当接受肠内营养时乳酸浓度增加，这就需要紧急寻找非闭塞性肠系膜缺血的原因，并调整肠内营养（减少、停止和/或转为肠外营养或早期耐受营养限制）。应寻找非闭塞性肠系膜缺血的早期迹象，以便在发生不可逆转的壁间坏死之前迅速做出诊断。在诊断出急性肠系膜缺血后，应主要目标是改善肠道氧供需平衡，评估肠道缺血的可逆性，并在发生不可逆转的壁间坏死时紧急进行切除术。急性肠系膜缺血缓解后，应评估重新引入肠内营养的获益风险分析。
