why is serum lactate elevated in sepsis?
In sepsis, lactate is bad and needs to be corrected immediately via aggressive fluid resuscitation, right?
Well, maybe. But it’s complicated.
A brief thread on lactate in sepsis!
Elevated lactate is most commonly attributed to hypoperfusion 2/2 hypotension and we usually give fluid in response.
However, it can also be thought of as a reflection of endogenous epinephrine production, which stimulates aerobic glycolysis via beta-2 adrenergic receptors.
And lactate isn’t all bad!
Lactate may serve as a protective metabolic fuel for the heart and brain during stress.
Still, lactate can help identify patients in shock who have a strong endogenous catecholamine response, indicating they need more intensive care.
The role of trending lactate levels in sepsis resuscitation is unclear – MAP and UOP are likely better.
However, persistent elevation should draw extra attention to your management – notably your abx selection, if you have source control, and other possible etiologies.
DDx for lactatemia:
Type A (tissue hypoxia)
– local ischemia (mesenteric, limb)
– decreased oxygenation
– increased adrenergic state (albuterol, cocaine, epinephrine)
– decreased krebs (thiamine deficiency, EtOH)
– liver dysfunction
Note that sodium lactate administration, as in lactated ringers, is safe and potentially beneficial.
It’s unlikely to lead to an elevated lactate level.
Moreover, epinephrine, previously avoided due to concerns about lactate generation, should be considered as a second-line vasopressor in septic shock.
At low doses, it acts as an inotrope, and at higher doses, it also acts as a vasoconstrictor.