TY - JOUR
T1 - Natural History of Lactic Acidosis after Grand-Mal Seizures
T2 - A Model for the Study of an Anion-Gap Acidosis Not Associated with Hyperkalemia
AU - Orringer, Carl E.
AU - Eustace, John C.
AU - Wunsch, Christian D.
AU - Gardner, Laurence B.
PY - 1977/10/13
Y1 - 1977/10/13
N2 - To define the time course of the metabolic acidosis that follows a single grand-mal seizure, we obtained serial blood samples from eight consecutive patients. Immediately after a seizure, the mean (± S.E.M.) venous lactate concentration was 12.7±1.0 meq per liter, the mean carbon dioxide content 17.1±1.1 nmol per liter, and the mean arterial pH 7.14±0.06. Sixty minutes later their values were 6.6±0.7 meq per liter (P<0.005), 23.6±1.1 mmol per liter (p<0.005) and 7.38±0.04 (P<0.005) respectively. The spontaneous resolution of the acidosis was due, in large part, to the metabolism of lactate and to the concomitant removal of hydrogen ion. There was no change in the serum potassium concentration, despite the development of a severe systemic acidemia and the subsequent return to normal of the pH. We suggest that the patient with seizures may serve as a unique model of lactic acidosis.
AB - To define the time course of the metabolic acidosis that follows a single grand-mal seizure, we obtained serial blood samples from eight consecutive patients. Immediately after a seizure, the mean (± S.E.M.) venous lactate concentration was 12.7±1.0 meq per liter, the mean carbon dioxide content 17.1±1.1 nmol per liter, and the mean arterial pH 7.14±0.06. Sixty minutes later their values were 6.6±0.7 meq per liter (P<0.005), 23.6±1.1 mmol per liter (p<0.005) and 7.38±0.04 (P<0.005) respectively. The spontaneous resolution of the acidosis was due, in large part, to the metabolism of lactate and to the concomitant removal of hydrogen ion. There was no change in the serum potassium concentration, despite the development of a severe systemic acidemia and the subsequent return to normal of the pH. We suggest that the patient with seizures may serve as a unique model of lactic acidosis.
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U2 - 10.1056/NEJM197710132971502
DO - 10.1056/NEJM197710132971502
M3 - Article
C2 - 19702
AN - SCOPUS:0017694171
VL - 297
SP - 796
EP - 799
JO - New England Journal of Medicine
JF - New England Journal of Medicine
SN - 0028-4793
IS - 15
ER -