Lactic acidosis (LA) is frequently observed in critically ill patients. In patients with diabetic ketoacidosis (DKA), multiple pathophysiological mechanisms are accountable for the elevated lactate concentrations. The precise mechanism is uncertain, but the compromised tissue perfusion due to hypovolemia, an epinephrine-driven response due to insulin insufficiency, the impact of stress status, and glycogenic hepatopathy (GH) are involved. GH can cause lactic acidosis, a rare condition due to excessive glycogen accumulation in the hepatocytes, and also an uncommon complication from poorly managed diabetes mellitus (DM), characterized by hepatomegaly and temporary elevation in serum aminotransferase enzyme levels.
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Lopez et al. (2024) studied this question.
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