Lactic Acidosis

Lactic acidosis is a raised anion gap metabolic acidosis caused by lactate accumulation, and is the commonest cause of severe metabolic acidosis in hospital practice.

It is conventionally divided into two types, and the distinction is clinically useful because it directs the search for a cause:

• Type A results from tissue hypoperfusion or hypoxia: shock of any cause, sepsis, cardiac arrest, severe hypoxaemia, severe anaemia, mesenteric ischaemia, limb ischaemia, and carbon monoxide or cyanide poisoning. This is the common and dangerous group

• Type B occurs without evident hypoperfusion, and includes liver failure (impaired lactate clearance), malignancy, thiamine deficiency, and drugs and toxins: notably metformin, alcohol, salicylates, antiretrovirals, propofol and linezolid

Lactate is one of the most useful prognostic markers in acute medicine: the trend matters more than the absolute value, and failure of lactate to clear with treatment is a strong marker of ongoing hypoperfusion and poor outcome.

• Serum lactate, on a venous or arterial sample; venous lactate is adequate for screening and correlates acceptably with arterial. A raised lactate should be repeated to assess clearance, since a single value says far less than the trajectory
• Blood gas confirming raised anion gap metabolic acidosis
• Assess perfusion clinically and haemodynamically to separate type A from type B: blood pressure, capillary refill, urine output, mental status, and mottling
• Directed investigations for the cause: infection screen and cultures, ECG and troponin, imaging for mesenteric ischaemia where abdominal pain is out of proportion to findings, haemoglobin, and toxicology
• Liver function, since impaired clearance both causes and sustains hyperlactataemia
• Metformin should be specifically sought in the drug history in any patient with severe lactic acidosis and renal impairment; metformin-associated lactic acidosis is uncommon but carries high mortality and is a dialysis indication
• Thiamine deficiency is a treatable and easily missed cause, particularly in alcohol use disorder, malnutrition and after bariatric surgery
• Recognised pitfalls: ethylene glycol poisoning can cause a falsely elevated lactate on some point-of-care analysers, through interference from glycolate; and D-lactic acidosis in short bowel syndrome is not detected by standard L-lactate assays

• Restore tissue perfusion, which is the definitive treatment for type A and takes precedence over everything else: fluid resuscitation guided by response, vasopressors where fluid alone is insufficient, source control and antimicrobials in sepsis, and revascularisation for ischaemia
• Oxygenation and ventilatory support as required
• Treat the specific cause: antidotes for cyanide and carbon monoxide, discontinuation of the offending drug, and haemodialysis for metformin-associated lactic acidosis, which both removes metformin and corrects the acidosis
• Thiamine, given empirically where deficiency is plausible; it is cheap, safe, and the response can be rapid and dramatic in genuine deficiency
• Bicarbonate is not routinely recommended in lactic acidosis and has not been shown to improve outcomes. It may be considered at severe acidaemia (pH below approximately 7.1), particularly with acute kidney injury, but the priority remains correcting perfusion rather than the number
• Monitor lactate clearance as a marker of treatment response, typically every 2–4 hours in the acute phase. A falling lactate indicates improving perfusion; a static or rising lactate despite apparently adequate resuscitation should prompt reassessment for an unaddressed cause, particularly ischaemia, an undrained source of sepsis, or a toxic cause
• Avoid attributing a persistently raised lactate to a benign cause without first excluding the dangerous ones

Referral: critical care for any significant lactic acidosis with haemodynamic compromise; surgery urgently for suspected mesenteric or limb ischaemia; nephrology for dialysis in metformin-associated lactic acidosis.