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Blood lactate has become easy to measure, with results now readily available to us in clinical practice from point-of-care testing and blood gas analysers. It has long been recognised that hyperlactataemia in acutely unwell patients is associated with poorer outcomes,1 but its interpretation and clinical significance is not always clear. In this review article, we present the evidence for the use of lactate as a diagnostic and therapeutic marker in acutely unwell children.
Lactate (2-hydroxypropanoic acid) is produced by glycolysis—glucose oxidation—from pyruvate, via the enzyme lactate dehydrogenase, which is located in the inner mitochondrial membrane.2 The terms ‘lactate’ and ‘lactic acid’ are often used interchangeably, but strictly speaking, at physiological pH, lactic acid is almost completely dissociated from its protons.3 The name originates from its initial discovery, in 1780, from samples of sour milk, and it was first isolated from blood in 1843 from women who died from puerperal sepsis.4 ,5 Historically, lactate was considered to be a ‘waste product’ of anaerobic metabolism and assumed to be a surrogate marker for tissue perfusion.1 However, more recent evidence has challenged these classic views. Lactate is now understood to be a valuable metabolic fuel, not necessarily associated with dysoxia, particularly in energy-intense organs such as the brain and skeletal muscle.6 ,7 It also plays an important role in cell signalling, via transporter proteins which shuttle lactate between cells.7 ,8 The familiar classification of lactic acidosis into type A (associated with hypoxia) and type B (in the absence of hypoxia)9 is somewhat limited, and fails to address the complexity of its physiology.
Lactate is continually produced and turned over rapidly, even at rest,4 ,8 and baseline blood levels of 0.5–1.8 mmol/L reflect the global balance between lactate production and consumption.10 …
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