lactateacidosis

Lactic acidosis, sometimes written as lactate acidosis, is a form of metabolic acidosis defined by elevated blood lactate levels and acidemia resulting from excess lactate production or impaired clearance. Lactate is produced from pyruvate during glycolysis, and under normal conditions is cleared mainly by hepatic gluconeogenesis and, to a lesser extent, by the kidneys. When production outpaces clearance, lactate accumulates and contributes to an anion gap metabolic acidosis.

Classification and causes: Type A lactic acidosis results from tissue hypoperfusion or hypoxia (for example shock, severe anemia, cardiogenic or septic shock). Type B lactic acidosis occurs despite adequate oxygen delivery and is subdivided into B1 disease-related (e.g., liver disease, diabetes mellitus, cancer), B2 drug or toxin–induced (e.g., metformin, ethanol, salicylates), and B3 mitochondrial dysfunction (e.g., inherited mitochondrial diseases).

Clinical features depend on the underlying cause and can range from signs of shock to nonspecific symptoms such as malaise or abdominal pain. Laboratory findings typically include elevated lactate and an increased anion gap metabolic acidosis; lactate concentration is commonly >2 mmol/L, with higher levels correlating with severity. Lactate-to-pyruvate ratio and lactate clearance can aid in etiologic assessment.

Management focuses on treating the underlying cause and supporting tissue perfusion and oxygenation. This includes fluid resuscitation, vasopressor support when needed, oxygen therapy, and treatment of sepsis if present. Discontinuation of offending drugs is important (for example metformin in renal impairment). Renal replacement therapy may be considered in severe cases or in metformin-associated lactic acidosis. Bicarbonate therapy is controversial and reserved for severe acidemia.

Prognosis depends on the etiology and severity; persistent or extreme hyperlactatemia is associated with higher mortality.

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