ALTHOUGH endogenous lactic acid has been recognized as a source of metabolic acidosis for many years in a variety of situations,1-5 it was not until the publication by Huckabee of his clinical observations of the significance of lactic acid acidosis 6,7 that great interest was stimulated in this condition. The demonstration that severe metabolic acidosis, frequently of fatal outcome, was a significant clinical problem has led to the increasing recognition of this situation in clinical practice.5,8-17 The definition of lactic acidosis remains arbitrary. Since the production of lactate is always accompanied by an equivalent appearance of hydrogen ion, significant elevation in blood lactate must be interpreted as lactic acidosis regardless of resultant arterial pH or bicarbonate levels. Qualifying factors include the degree of compensation for the metabolic acidosis, represented by arterial pH, eventual outcome (survival or fatality), the presence or absence of clinical symptoms of metabolic acidosis,