To the Editor:
We read with great interest the recent review discussing the clinical interpretation of lactate measurements by Drs. Pino and Singh.1 The article covered the topic in great detail; however, there are several points which we also feel warrant inclusion when discussing this topic.
An additional source of lactate in surgical patients can be from red blood cell transfusion. As the authors state, red cells are completely anaerobic because they lack mitochondria and require glycolysis for maintenance of adenosine triphosphate. As a result, stored red blood cells are a source of lactate from transfusions; lactate levels and resultant patient lactate loads can increase with the use of stored red blood cells. Although many patients have adequate capability to metabolize lactate loads from transfusion, this may not be the case in massive transfusions, liver transplantation, or pediatric cardiac surgery. In particular, sudden massive boluses of red blood cell–derived lactate in pediatric cardiac surgery from older stored red blood cells can significantly impact more traditional and conventional interpretations of lactate concentration.2
Additionally, endogenous overproduction of lactate may represent more than a metabolic waste product. Proponents of the concept contend that lactate can function as a metabolic glucose regulator and regulator of insulin release and insulin resistance.3 Brooks4 reviews compelling evidence that endogenous L-lactate is actively involved in aerobic intermediary energy metabolism and signaling effects through hydroxycarboxylic acid receptor 1. In the population with obesity, new evidence suggests hormonally triggered overproduction of lactate is an essential and obligatory feature of adipocytes, even in the absence of hypoxia.5 Adipocyte lactate production may therefore alter interpretations of elevated lactate levels in obesity and insulin resistance, although this concept is too recent for correlative studies in the perioperative period to define the magnitude and significance of these metabolic pathways.
The authors state that typical measurements of lactate, as conventionally performed with a blood gas machine, do not detect D-lactate, which has been shown to produce numerous deleterious effects. Some formulations of lactated Ringer’s solution have historically contained DL lactate,6 and although most formulations today are likely to contain only L-lactate, compositions may vary between countries and manufacturers. Additionally, although the consumption of fermented foods may contribute only a small proportion of total lactate as D-lactate, the presence and significance of D-lactate in pathologic states is not limited to gut ischemia or short bowel syndrome. Small intestinal bacterial overgrowth, in the absence of short bowel syndrome, has been associated with D-lactic acidosis with central nervous system symptoms. In fact, half of probiotic strains have been shown to ferment carbohydrates to D or DL lactate and may be responsible for gastrointestinal and central nervous system symptoms from D-lactic acidemia in some patients.7 Because D-lactate levels are not customary measurements, it is conceivable that many cases can be missed with routine laboratory investigations.
The authors declare no competing interests.