There are several ways to classify lactic acidosis. The classical system separates lactic acidosis according to its pathology, whereas more novel systems classify it according to physiology. The attractiveness of the incumbent system lies in its simplicity, rather than its validity. Its categories are however flawed when it comes to categorising complex pathophysiological processes, such as septic shock. In counter-argument, new classification systems are equally bad at classifying complex disorders. They seize the advantage of pathophysiological completeness and gain in explanatory power while sacrificing simplicity and memorability.
The artificial classification of lactic acidosis proposed by Cohen and Woods in 1983 has persisted in spite of questionable utility in critical care. They divided the causes of lactic acidosis into two camps: Type A (lactic acidosis due to impaired tissue perfusion) and Type B (lactic acidosis with adequate tissue perfusion).
Type B was further subdivided into type B1, B2 and B3. Type B1 lactic acidosis was said to be as a result of “disease states”; Type B2 was said to be drug-related, with some drug effect interfering with carbohydrate metabolism. Type B3 was said to be the consequence of inborn errors of carbohydrate metabolism.
In clinical reality, several of these tend to co-exist. For instance, in septic shock there are several Type A and Type B mechanisms taking effect.
A much better, and more clinically useful, classification system has appeared in an article by Phypers & Pierce (2006), which is available for free online. Because the classical Cohen and Woods classification is well-known, it remains on the menu; however for the purposes of organizing my own thoughts, I have also reproduced the alternative 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
Why is this classification more relevant? In my opinion, it hints at the solutions the the problem. To decrease the amount of lactate, one would need to either decrease production (by addressing the cause of the problem) or to improve clearance.
The solutions to the various causes of over-production of lactate, being numerous, are specific to the problems. As for the clearance - well. The hepatic clearance impairment due to liver disease is not something one can hope to address without either transplanting the liver or improving hepatic blood flow (in the course of improving blood flow in general). The renal resorption threshold is not amenable to manipulation, but once it has been reached one can expect increased glomerular filtration to improve renal clearance of unresorbed lactate. Additionally, one can improve clearance by using the artificial glomerulus of dialysis.
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.