Lactate: the Black Peter in high-risk gastrointestinal surgery patients

J Thorac Dis 2016;8(6):E440-E442 jtd.amegroups. com Lactate arises from metabolisation of glucose to pyruvate. Pyruvate either is transformed to or from lactate in the cytosol or converted by pyruvate dehydrogenase in mitochondria to acetyl coenzyme A which enters the Krebs cycle to produce energy for cellular metabolism. Any switch to anaerobic metabolism will reduce activity of the highly oxygen-dependent Krebs cycle and shunt “redundant” pyruvate towards lactate (1). Why is this seemingly trifle lactate molecule so important in the intensive care unit (ICU)? Increased blood lactate concentrations are dreaded by ICU physicians since they are almost invariably linked to the presence or persistence of inadequate tissue perfusion and oxygenation. Hyperlactatemia at a cut-off value between 2 and 4 mmol/L is associated with worse outcome in all types of shock. As such, the blood lactate level has become a powerful “biomarker” to predict morbidity and mortality as well as a tool to guide resuscitation in hemodynamically compromised critically ill patients (2). However, lactate may also be produced independently from tissue hypoxia in conditions characterized by decreased pyruvate dehydrogenase activity (e.g., thiamine deficiency), modification of the cellular redox potential (e.g., ketoacidosis, ethanol abuse), or accelerated glycolytic flux (e.g., induced by drugs such as catecholamines and biguanides) (3). Monitoring lactate has been progressively introduced in the postoperative setting. Blood lactate concentration proved to be an indispensable and accurate marker of mortality at both individual patient and patient cohort level after cardiac surgery (4). An early lactate increase was also found to predict complications after elective pancreatic (5) and extensive liver surgery (6). However, the association between lactate concentrations and mortality with regard to type of gastrointestinal (GI) surgery (emergency vs. elective) remained unexplored. Hyperlactatemia following elective GI surgery was intuitively accepted as a relatively “physiological” reaction to surgical stress. Indeed, a GI surgical intervention itself will cause activation of coagulation and inflammatory pathways which can be further accentuated by procedure-related gut manipulation, temporary ischemia, and eventual bacterial translocation and shedding. In contrast, elevated lactate during emergency GI surgery was traditionally linked to a more frequent occurrence of peri-operative hemodynamic instability and resuscitation-associated ischemia-reperfusion disorders. Li et al. studied dynamic postoperative changes in blood lactate levels during the first 24 h after elective major abdominal surgery. They found that time-weighted average lactate at a cut-off level as low as 1.5 mmol/L was independently predictive of both overall and major postoperative complications observed in nearly half of the patients (7). These findings have now been corroborated and expanded by the recently published study of Creagh-Brown et al. in Critical Care Medicine. These investigators showed that the highest lactate level obtained on the first day after ICU admission in patients who underwent major GI surgery was independently associated with increased morbidity and in-hospital mortality. This association was not related to the type of intervention (emergency vs. elective) and also continued down into the “normal lactate concentration” range (8). The key message of Creagh-Brown et al. is that any increase in postoperative lactate after high-risk GI surgery is a “bad” prognostic sign. It can be assumed that Commentary