LACTIC ACIDOSIS.

Abstract

LACTIC ACID, long recognized as an important product of normal metabolism,42 was first associated with a metabolic acidosis by Barr, Himwich and Green in 1924.9,10 These investigators recognized metabolic acidosis following strenuous physical exercise and linked it with the observed accumulation of blood lactic acid. They called the condition "lactic acid acidosis." Following that report, sporadic references have been made to lactic acid as a demonstrated or suspected cause of metabolic acidosis in a variety of conditions. These have included the demonstrations of increased lactate accompanying the acidosis of diarrheal dehydration in infants,23 anoxia,* muscular exercise,t hemorrhagic and endotoxin shock,: glycogen storage disease,70'103 inadequate blood flow during cardio-pulmonary bypass procedure,7 100 hyperthermia,43 hyperventilation,33'76'80 guanidine intoxication,99 methyl alcohol poisoning,13 salicylate intoxication,36 nonketotic diabetic acidosis,4,24,9O,113 paraldehyde intoxication,62 and feeding of lactic acid milk to infants.52 It was not until the introduction of the clinical concept of lactic acidosis by Huckabee, in 1961,77'78 that it was recognized that severe metabolic acidosis related to the accumulation of large amounts of 'lactic acid in body water was of real clinical significance. Since Huckabee's initial report of nine patients with lactic acidosis, at least 62 additional cases have been reported.§ This presentation will concern itself with the entity of lactic acidosis, and will deal with current concepts of the mechanisms