Synopsis
Recognise a raised-anion-gap metabolic acidosis, identify lactate and other unmeasured acids, and reverse tissue hypoperfusion or toxic and metabolic causes before severe acidemia compounds organ failure.
- Metabolic acidosis is a low-bicarbonate process; respiratory compensation lowers carbon dioxide but never cures the underlying acid burden.
- Calculate the anion gap from the local laboratory values, commonly sodium minus chloride plus bicarbonate, and interpret it against the laboratory range and serum albumin.
- A low albumin can conceal clinically important unmeasured acid, so an apparently normal gap does not exclude lactate, ketones, renal acids or toxins in a critically ill patient.
- Lactic acidosis describes raised lactate with acid-base disturbance, not every mildly raised lactate; trend, perfusion and the clinical cause matter more than one isolated number.
- Type A hyperlactataemia reflects impaired oxygen delivery or utilisation in shock, hypoxaemia, anaemia or regional ischaemia, whereas type B causes include medicines, liver dysfunction, seizures, thiamine deficiency and malignancy.
- A raised gap with normal lactate should trigger targeted testing for beta-hydroxybutyrate, renal failure, salicylate, toxic alcohols and other causes; never label every gap as lactic acidosis.
- Venous blood gas usually provides rapid pH, bicarbonate and lactate information; use an arterial sample when arterial oxygenation or a precise respiratory assessment is required.
- Treat perfusion and the cause: controlled crystalloid, source control and antimicrobials for sepsis, insulin-based JBDS treatment for DKA, antidote or dialysis pathways for selected toxins, and surgery for ischaemic bowel.
- Sodium bicarbonate is not routine treatment for lactic acidosis and can add sodium, carbon dioxide and volume; reserve it for defined specialist-led indications under the current local critical-care or toxicology protocol.
Key red flags
Hypotension, mottling, prolonged capillary refill, cool peripheries, confusion and oliguria with rising lactate indicate threatened organ perfusion even when a single blood pressure appears acceptable.
Deep rapid respiration may be physiological compensation for metabolic acidosis. Sedation or exhaustion can remove compensation and cause abrupt pH deterioration, so airway decisions require senior critical-care planning.
Severe abdominal pain out of proportion, gastrointestinal bleeding, limb pain with absent pulses or evolving compartment signs can generate lactate before global shock becomes obvious.
Vomiting, dehydration, abdominal pain, diabetes, starvation, pregnancy or heavy alcohol use with raised blood beta-hydroxybutyrate suggests ketoacidosis; glucose may be modest with SGLT2 exposure or pregnancy.
Severe illness, acute kidney injury, hypoxia or shock in a person taking metformin can permit accumulation and lactic acidosis, but clinicians must still find and treat the precipitating disease.
Visual disturbance, inebriation, renal injury, hypocalcaemia or unexplained high osmolar and anion gaps suggests methanol or ethylene glycol exposure and requires immediate poisons and renal advice.
Investigation priorities
Confirm acidemia, bicarbonate reduction, respiratory compensation and current lactate rapidly.
Management branches
Raised lactate accompanied by hypotension, hypoperfusion, altered consciousness or organ dysfunction.
- Start ABCDE, high-acuity monitoring, intravenous access and urgent blood gas, glucose, ketones, electrolytes and cultures while calling senior and critical-care support.
- Give controlled crystalloid boluses with repeated response assessment, oxygen only to the appropriate target, and early vasopressor support through critical care when shock persists.
- Treat the cause in parallel: follow NICE sepsis timing and source control, control haemorrhage, restore flow to an ischaemic limb or bowel, and correct severe hypoxaemia or anaemia as indicated.
- Trend lactate, pH, urine output, mental state and peripheral perfusion, stopping ineffective fluid loading and escalating when physiology or organ function fails to improve.