Metabolic acidosis in the critically ill: part 2. Causes and treatment.
The correct identification of the cause, and ideally the individual acid, responsible for metabolic acidosis in the critically ill ensures rational management. In Part 2 of this review, we examine the elevated (corrected) anion gap acidoses (lactic, ketones, uraemic and toxin ingestion) and contrast them with nonelevated conditions (bicarbonate wasting, renal tubular acidoses and iatrogenic hyperchloraemia) using readily available base excess and anion gap techniques. The potentially erroneous interpretation of elevated lactate signifying cell ischaemia is highlighted. We provide diagnostic and therapeutic guidance when faced with a high anion gap acidosis, for example pyroglutamate, in the common clinical scenario 'I can't identify the acid--but I know it's there'. The evidence that metabolic acidosis affects outcomes and thus warrants correction is considered and we provide management guidance including extracorporeal removal and fomepizole therapy.
Morris
C G
CG
Intensive Care Medicine and Anaesthesia, Derby Hospitals Foundation Trust, Derby Royal Infirmary, London Road, Derby DE1 2QY, UK. cmorris@doctors.org.uk
Low
J
J
D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000175:diagnosis / Q000209:etiology* / Q000628:therapy*; D000140:Acidosis, Lactic / Q000209:etiology / Q000628:therapy; D000141:Acidosis, Renal Tubular / Q000209:etiology / Q000628:therapy; D016638:Critical Illness; D006801:Humans; D011379:Prognosis