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:
- Type A (lactic acidosis due to impaired tissue perfusion)
- Type B (lactic acidosis with adequate tissue perfusion).
- Type B1 (lactic acidosis a result of “disease states”)
- Type B2 (drug-related)
- Type B3 ( the consequence of inborn errors of metabolism)
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:
- Manage the underlying cause of the lactic acidosis - and the precise management strategy obviously depends on the aetiology
- Increase the clearance of lactate artificially using CVVHDF (which is probably not a very effective strategy, and represents immature "lactate-centric" management).
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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.
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