Lactate, Lactate, Lactate…
Question: “What are some causes of lactic acidosis?”
Lactate is one of those things we care so much about—but sometimes don’t give enough attention. And believe it or not…it comes in TWO flavors.
Type I/A Lactate: Due to hypoperfusion and hypoxia, when there is a mismatch between oxygen consumption and oxygen delivery. This leads to anaerobic respiration! This is what we always think about when we hear “elevated lactate”—a shock state.
Type II/B Lactate: This occurs when the mitochondria is unable to process the amount of pyruvate it is presented (for a reason other than hypoxia/hyoperfusion), the body is having trouble clearing this lactate, or the NAD/NADH ratio favors the production of lactate over pyruvate
Some causes include:
Thiamine Deficiency
Ethanol Intoxication
Malignancy
Metformin
Epinephrine
Liver Disease
Beta-Agonism
In the setting of longstanding alcohol use (perhaps for example in someone who tolerates an ETOH level of 400), hepatic dysfunction can disrupt lactate utilization. Longstanding ETOH use can also change the NAD/NADH ratio, favoring lactate. Acute intoxication has conflicting data.
Question: “What’s the use of lactate after seizure?”
Studies mostly focus on syncope vs seizure vs other reason for transient loss of consciousness. We don’t have a good cutoff for what counts as a suggestive lactate elevation.
Serum lactate appears to peak instantaneously after a seizure and rapidly clears, making it ineffective as a test after 1.5 hours. There may be some discriminating power, but the best cut-off is unclear and studies are all retrospective with specificities in the 80’s and sensitivities between 65-85%. In certain patient populations with other underlying medical comorbidities such as liver disease or sepsis, they may present with an elevated lactate and have delayed lactate clearance. Data is limited…but a very high lactate within 1.5hrs of seizure that clears completely after 1.5hrs is highly suggestive of a true seizure.
Cheers,
Dillon
