Definition and epidemiology
Lactic acidosis is a high-anion-gap metabolic acidosis driven by lactate accumulation, conventionally defined by a blood lactate above ~4–5 mmol/L with acidaemia. It is the most common cause of metabolic acidosis in critically ill children and a marker of disease severity across shock, sepsis, and inborn errors of metabolism. The classic split is into type A (lactate overproduction from tissue hypoperfusion/hypoxia) and type B (impaired clearance or aerobic overproduction without overt hypoperfusion), recognising that the two frequently overlap.
Clinical features
Type A presents in the context of its cause: the cool, mottled, tachycardic, oliguric child of hypovolaemic, cardiogenic, or septic shock, or after a hypoxic-ischaemic insult. Type B is more insidious — it should be considered when lactate is high but perfusion looks adequate. In paediatrics this raises inborn errors of metabolism (mitochondrial disease, organic acidaemias, fatty-acid oxidation and glycogen-storage disorders), as well as toxins and drugs, thiamine deficiency, malignancy, and hepatic dysfunction. Tachypnoea (respiratory compensation), altered mental status, and failure to thrive or recurrent decompensation in a young child are clues.
Diagnosis
Workup begins with a blood gas and anion gap (corrected for albumin in the hypoalbuminaemic, critically ill child), lactate, glucose, ketones, and renal/hepatic panels. Distinguish type A by evidence of hypoperfusion or hypoxia and treat the cause. When perfusion is adequate, pursue type B and metabolic disease: send urine organic acids and a plasma acylcarnitine profile, and use ancillary clues — hypoglycaemia with a “Reye-like” picture suggests fatty-acid oxidation defects; metabolic acidosis with characteristic organic acids suggests propionic or methylmalonic acidaemia; rash/alopecia suggests biotinidase or holocarboxylase deficiency; and the lactate/pyruvate ratio helps separate pyruvate-handling from respiratory-chain disorders. Always review medications and toxins.
See the full criteria: Lactic Acidosis
Red flags
- Lactate rising despite resuscitation — failed source control or ongoing hypoperfusion
- High lactate with apparently adequate perfusion — pursue type B / metabolic disease
- Hypoglycaemia with acidosis in an infant — possible inborn error of metabolism
- Severe acidaemia with haemodynamic instability or depressed consciousness
- Recurrent unexplained metabolic crises — refer to metabolic specialists
Management overview
The priority is to treat the underlying cause, not the number: restore perfusion and oxygen delivery in type A with volume resuscitation and haemodynamic support, source control and antimicrobials in sepsis, and stop or reverse offending drugs/toxins in type B. For suspected metabolic disease, stabilise with adequate dextrose-containing fluids to halt catabolism, give empiric thiamine where deficiency or a mitochondrial process is plausible, and involve metabolic specialists early — with cofactor and emergency-regimen decisions made by that team. Bicarbonate is contentious and reserved for selected cases of severe acidaemia; renal replacement may be needed for refractory acidosis or toxin clearance. Trend lactate as a marker of response while continuing to address the primary process.
References
- Kraut JA, Madias NE. Lactic Acidosis. N Engl J Med. 2014.
- Merck Manual Professional Edition. Lactic Acidosis.
- Foucher CD, Tubben RE. Lactic Acidosis. StatPearls, NCBI Bookshelf.
Decision support for qualified clinicians only — verify against current primary guidelines and your clinical judgement.