Outline the causes, and the principles of management of lactic acidosis in the critically ill.
• Causes can be divided into increased lactate production (including enhanced pyruvate production, reduced pyruvate conversion to CO2 & water or glucose, or preferential conversion of pyruvate to lactate), and diminished lactate utilisation.
• Most causes in the critically ill are due to the many causes of tissue hypoperfusion [Type A] (resulting in increased production and decreased utilisation), or decreased utilisation due to liver disease (especially with use of lactate containing fluids in renal replacement therapy). Other common causes include seizures, beta-2 adrenergic agonists (eg. adrenaline and salbutamol), metformin (uncertain mechanism) and post-cardiac surgery. Consider also d- lactic acidosis associated with the short bowel syndrome.
• Principles of management include correcting hypoperfusion (fluids, inotropes, vasopressors), and if possible, correction of underlying disorder (treat seizures, shivering, glucose abnormalities, etc.) and removal of offending drugs (including metformin, adrenaline, renal replacement fluid).
Causes of lactic acidosis are discussed at length in another chapter.
In brief, one may classify it according to several classification systems, of which the Cohen-Woods classification is for some reason the more popular.
The Cohen-Woods classification is as follows:
Causes of lactic acidosis can be better classified according to the lesser-known (but biochemically superior) Phuypers and Pierce system:
Increased rate of glycolysis due to lack of ATP
Increased rate of glycolysis due to exogenous pro-glycolytic stimulus
Unregulated substrate entry into glycolysis
Pyruvate dehydrogenase inactivity
Defects of oxidative phosphorylation
Decreased lactate clearance
The approach to the management of lactic acidosis can be divided into two main approaches:
Narins RG, Krishna GG, Yee J, Idemiyashiro D, Schmidt RJ: The metabolic acidoses. In: Maxwell & Kleeman's Clinical Disorders of Fluid and Electrolyte Metabolism, edited by Narins RG, New York, McGraw-Hill, 1994, pp769 -825
Luft FC. Lactic acidosis update for critical care clinicians. J Am Soc Nephrol 2001 Feb; 12 Suppl 17 S15-9.
Ohs manual – Chapter 15 by D J (Jamie) Cooper and Alistair D Nichol, titled “Lactic acidosis” (pp. 145)
Cohen RD, Woods HF. Lactic acidosis revisited. Diabetes 1983; 32: 181–91.
Reichard, George A., et al. "Quantitative estimation of the Cori cycle in the human." Journal of Biological Chemistry 238.2 (1963): 495-501.
Andres, Reubin, Gordon Cader, and Kenneth L. Zierler. "The quantitatively minor role of carbohydrate in oxidative metabolism by skeletal muscle in intact man in the basal state. Measurements of oxygen and glucose uptake and carbon dioxide and lactate production in the forearm." Journal of Clinical Investigation 35.6 (1956): 671.
Phypers, Barrie, and JM Tom Pierce. "Lactate physiology in health and disease." Continuing Education in Anaesthesia, Critical Care & Pain 6.3 (2006): 128-132.