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.
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.
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.
Key medicines
Balanced isotonic crystalloidGive cautious protocol-led boluses with bedside reassessment after each aliquot rather than an automatic large volume.
Empirical antimicrobial therapyAdminister the current local sepsis regimen at the NICE-defined urgency after appropriate cultures when feasible.