With the advent of sepsis protocol masterminding, lactate has elbowed out the white blood cell count along with other parameters to become our primary measure of badness. But as we all know, while lactate elevation may indicate the severity of a patient’s sepsis, not all lactate elevations are due to sepsis. Let’s take a minute to remind ourselves of other reasons our patient might have a lactic acidosis.

[spacer height=”20px”]The two basic physiologic causes are increased lactate production – via increased pyruvate production, decreased pyruvate conversion, or preferred pyruvate conversion to lactate – and decreased lactate utilization/excretion.
[spacer height=”20px”]More specifically, we can break down lactic acidosis into Type A/decreased oxygen delivery and Type B/no signs of decreased oxygen delivery, although remember this can be a tad slippery in terms of overlap:
[spacer height=”20px”]TYPE A:
[spacer height=”20px”]1. Decreased perfusion
general – e.g. all causes of shock (distributive, obstructive, cardiogenic, hypovolemic), cardiac arrest
regional – e.g. mesenteric ischemia, burns, limb ischemia
2. Anaerobic muscle activity – e.g. seizure
3. Decreased oxygen delivery – e.g. anemia
4. Decreased oxygen utilization – e.g. carbon monoxide or CN poisoning
[spacer height=”20px”]TYPE B:
[spacer height=”20px”]B1: Underlying disease
-e.g. malignancy, short bowel syndrome, renal and hepatic failure, diabetes/DKA
B2: Medications and toxins
-e.g. alcohols, metformin, salicylates, INH, beta-agonists, epinephrine
B3: Inborn errors of metabolism
-e.g. pyruvate dehydrogenase deficiency
[spacer height=”20px”]If you don’t enjoy the Type A/B breakdown, then here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3975915/table/T1/
[spacer height=”20px”]Great source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3975915/
[spacer height=”20px”]Image taken from: extremephillyfishing.blogspot.com